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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":623,"VI":624},"\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">04\u002F10\u002F2015 Ministry of Information and Communications allowed Can Tho journal of medicine and pharmacy to operate (102 \u002FGP-BTTTT)\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">07\u002F16\u002F2015 Can Tho journal of medicine and pharmacy is internationally recognized: ISSN 2354-1210\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">In 2016, The journal has been included in the list of medical science journals by The State Council for professorship which is awarded a work score of 0-0.5 points for a published article.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Can Tho Journal of Medicine and Pharmacy welcome original works that haven’t been submitted or published in other medical journals. Posts must contain content related to one of the journal’s categories.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The content published\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The journal is divided into 3 categories:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Scientific research article: are valuable scientific works, which have been researched and accepted.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Overview of medicine, biology and pharmacy: serving the objective of continuing training in the fields of medicine, biology and pharmacy; to systematize classical and modern knowledge.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Update information on new knowledge about medicine, biology, pharmacy in the country and in the world.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Scope\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Publication and introduction of scientific research in the fields:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Medicine (internal medicine, surgery, pediatrics, obstetrics and gynecology, odonto-stomatology, laboratory, oncology, traditional medicine, nursing).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Biology (genetics, biotechnology).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Pharmacology (pharmaceutics, drug quality analysis-control, synthetic pharmaceutical chemistry, biochemistry, pharmacognosy, botany, clinical pharmacy).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- To enhance the quality of undergraduate, postgraduate education, scientifically researching and meet the necessary treatment in hospital.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Introducing the updated domestic and oversea information about science technology to promote scientific research and exchanging technology in local, other universities.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Exchanging pharmaceutical and medical information for social health developing in the Mekong Delta and Vietnam.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The object\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Postgraduate students, student of Can Tho University of Medicine and Pharmacy, scientists from schools, research institutes, hospitals, health centers, pharmaceutical companies of the Mekong Delta; other provinces and regions in Vietnam and other country.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Address\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Headquarters of Can Tho Journal of Medicine and Pharmacy, located Scientific Research and International Cooperation Office: 179 Nguyen Van Cu Street, An Khanh Ward, Ninh Kieu District, Can Tho City, Vietnam.\u003C\u002Fspan>\u003C\u002Fp>","\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Ngày 16\u002F7\u002F2015, Tạp chí Y Dược học Cần Thơ được cấp chỉ số quốc tế: ISSN 2354-1210.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 4\u002F2016, Tạp chí đã được Hội đồng Giáo sư ngành Y đưa vào danh sách các tạp chí khoa học Y học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Năm 2020 Tạp chí Y Dược học Cần Thơ đã được phê duyệt vào danh mục của các Hội đồng Giáo sư ngành Dược học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ ra 12 số\u002Fnăm, 180-200 trang\u002Fsố.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 12\u002F2022 Tạp chí Y Dược học Cần Thơ là thành viên của hệ thống Crossref và từ tháng 01\u002F2023 tạp chí thực hiện bình duyệt online kín 2 chiều nhằm tăng tính minh bạch, tin cậy của các công trình nghiên cứu khoa học và đảm bảo tốt nhất chất lượng khoa học của bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ, mục đích và phạm vi của tạp chí\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ và mục đích hoạt động của tạp chí: xuất bản nhằm mục đích phổ biến kết quả từ các đề tài nghiên cứu khoa học; giao lưu trao đổi khoa học, chia sẻ kinh nghiệm, học tập, đồng thời cập nhật thông tin khoa học mới trong các lĩnh vực y, sinh, dược học trong và ngoài nước.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phạm vi của tạp chí: Tạp chí xuất bản được chia thành 3 chuyên mục: (i) Bài báo nghiên cứu khoa học là kết quả công trình nghiên cứu khoa học có giá trị đã được triển khai nghiên cứu, (ii) Bài tổng quan y, sinh, dược học: phục vụ mục tiêu đào tạo liên tục trong lĩnh vực y, sinh, dược học; nhằm hệ thống hóa những kiến thức kinh điển và hiện đại; (iii) Thông tin cập nhật kiến thức mới về y, sinh, dược học trong nước và trên thế giới.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Chính sách truy cập mở\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ áp dụng chính sách truy cập mở đối với các bài báo đã xuất bản đến với độc giả, nhằm mở rộng cơ hội tiếp cận các kết quả nghiên cứu chất lượng cao và tăng cường trao đổi kiến thức. Tạp chí đăng tải trực tuyến (miễn phí) toàn văn các bài báo được công bố trên website của Tạp chí (https:\u002F\u002Ftapchi.ctump.edu.vn).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đạo đức xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ cam kết tuân thủ đạo đức xuất bản phù hợp với các hướng dẫn và tiêu chuẩn của the Committee on Publication Ethics (COPE), tuân thủ các nguyên tắc của COPE’s Core Practices, Best Practices Guidelines for Journal Editors và Guidelines on Good Publication Practices.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Bản thảo bài báo chỉ được chấp nhận khi được tác giả chịu trách nhiệm chính cam kết các nội dung sau: Các nội dung của bản thảo chưa được đăng tải toàn bộ hoặc một phần ở các tạp chí khác; Tất cả các tác giả đều có đóng góp một cách đáng kể vào quá trình nghiên cứu hoặc chuẩn bị bản thảo và cùng chịu trách nhiệm về các nội dung của bản thảo; Tuân thủ các biện pháp đảm bảo đạo đức nghiên cứu (ví dụ thỏa thuận đồng ý tham gia nghiên cứu).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Cam kết bảo mật\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí cam kết thực hiện và tuân thủ các quy định của luật và các văn bản hướng dẫn liên quan đến bảo mật thông tin cá nhân trên không gian mạng. Các thông tin mà người dùng (tác giả, độc giả, biên tập viên, người phản biện) nhập vào các biểu mẫu trên Hệ thống Quản lý xuất bản trực tuyến của tạp chí chỉ được sử dụng vào các mục đích đã được tuyên bố rõ ràng và sẽ không được cung cấp cho bất kỳ bên thứ ba nào khác, hay dùng vào bất kỳ mục đích nào khác.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phí gửi bài\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng bài: 1.000.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng nhanh: 1.500.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với tác giả là cán bộ viên chức thuộc Trường Đại học Y Dược Cần Thơ thì được hỗ trợ 50% lệ phí gửi đăng bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với sinh viên thực hiện đề tài nghiên cứu khoa học cấp trường được hỗ trợ 100% lệ phí đăng bài ( Tác giả gửi đính kèm “ Quyết định về việc giao tổ chức thực hiện đề tài nghiên cứu khoa học cấp Trường của sinh viên”).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Hình thức nộp lệ phí:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Tiền mặt:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Nộp trực tiếp tại Phòng Tài chính - Kế toán, Trường Đại học Y Dược Cần Thơ, số 179 Nguyễn Văn Cừ, P. An Khánh, Q. Ninh Kiều, thành phố Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Chuyển khoản:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tên Tài khoản: Trường ĐHYD Cần Thơ, Số TK: 0111000115668, tại ngân hàng Vietcombank chi nhánh Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Thời gian: Áp dụng từ ngày 01\u002F02\u002F2023.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">* Phí gửi bài không được hoàn trả khi bài viết bị từ chối hoặc tác giả xin rút bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Quy trình phản biện bài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ thực hiện quy trình phản biện kín hai chiều nghiêm ngặt. Danh tính của những người phản biện không được tiết lộ cho các tác giả và ngược lại. Quy trình thẩm định bài báo đăng gồm các bước sau:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tiếp nhận bản thảo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tác giả liên hệ gửi bản thảo đến Tạp chí qua hệ thống trực tuyến tại website: https:\u002F\u002Ftapchi.ctump.edu.vn. Hướng dẫn về cách đăng ký, gửi bài và chuẩn bị bản thảo được cung cấp trên website của Tạp chí.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sàng lọc sơ bộ\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sau khi Tòa soạn nhận được bài báo của tác giả, Ban Thư ký sẽ tiến hành kiểm tra sơ bộ bài báo (các yêu cầu về nội dung và hình thức). Những bài báo không đúng quy cách hoặc có nội dung không phù hợp hoặc vi phạm bản quyền sẽ bị từ chối (Ban Thư ký thông báo phản hồi đến tác giả trong vòng 1 tuần). Những bài báo đủ điều kiện, được Ban Thư ký tòa soạn chuyển đến Ban Biên tập có cùng chuyên môn với nội dung bài báo để đề xuất người phản biện. Thời gian kể từ khi Ban Biên tập nhận bài báo đến khi đề xuất người phản biện bài báo chậm nhất là 5 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Vòng phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký gửi bài và yêu cầu phản biện đến 02 phản biện độc lập.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Các phản biện gởi nhận xét cho Ban Thư ký. Thời gian từ khi gửi bài cho phản biện đến khi nhận ý kiến của phản biện tối đa là 20 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xử ký kết quả phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Nếu ý kiến đồng ý cho đăng và không cần chỉnh sửa, Ban Thư ký tiếp tục đăng bài theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Nếu ý kiến đồng ý đăng và cần chỉnh sửa, Ban Thư ký sẽ thông tin đến tác giả chỉnh sửa theo yêu cầu của người phản biện. Thời gian chỉnh sửa và gửi lại kéo dài không quá 2 tuần, từ khi tác giả bài báo nhận được thông tin (Quá trình này có thể lặp lại tối đa 2 lần\u002F1 bài báo). Khi có sự thống nhất, đồng ý của người phản biện; bài báo được tiếp tục đăng theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Những bài báo có chất lượng không đạt yêu cầu, cả 2 phản biện không đồng ý cho đăng sẽ bị Tòa soạn từ chối đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký tổng hợp các bản thảo đã được tác giả hoàn thiện sau thẩm định trình Ban Biên tập xem xét, Tổng Biên tập phê duyệt, quyết định bài đăng theo các tiêu chí: sự phù hợp nội dung với tôn chỉ và mục đích, thể loại bài viết (ưu tiên các bài có bài có nghiên cứu chuyên sâu, hàm lượng khoa học cao), đóng góp mới bài báo, bài báo được ưu tiên đăng trong số gần nhất của Tạp chí theo thứ tự: tính thời sự, chất lượng bài báo và thời gian gửi bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Ban Biên tập và Ban Thư ký biên tập bản thảo, chế bản, đọc rà soát lỗi. Thời gian hoàn thành từ 10-15 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Ban Thư ký có trách nhiệm thông báo cho tác giả bài báo (bằng e-mail) về tình hình phê duyệt bài báo, thời gian, số kỳ, tập xuất bản bài báo theo qui định.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">4. Danh sách bài báo theo số Tạp chí được in ấn và phát hành trong năm định kỳ được công bố chính thức trên website: https:\u002F\u002Ftapchi.ctump.edu.vn\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>",{"VOID":626},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[630],{"id":631,"createTime":18,"updateTime":18,"relativeEntities":632,"slug":18,"properties":633,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":643,"parentIds":644,"statistic":18},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":634,"address":637,"country":640,"abbreviation":641},{"EN":635,"VI":636},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":638,"VI":639},"No 179, Nguyen Van Cu street, An Khanh ward, Ninh Kieu district, Can Tho city, Vietnam","Số 179, đường Nguyễn Văn Cừ, phường An Khánh, quận Ninh Kiều, thành phố Cần Thơ, Việt Nam",{"VOID":168},{"VOID":642},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":19,"impactFactorByYear":648,"i10Index":19,"i10IndexLast5Year":19,"totalPublication":650,"totalPublicationByYear":651,"totalCitation":656,"totalCitationByYear":657,"totalCitationPerPublication":257,"totalCitationPerPublicationByYear":659,"hindexLast5Year":195,"hindex":195},{"2022":649,"2023":260,"2024":255},0.01,1556,{"2020":197,"2021":652,"2022":653,"2023":654,"2024":655,"2025":270},57,306,801,358,161,{"2021":293,"2022":118,"2023":658},99,{"2021":660,"2022":458,"2023":253},0.23,{"impactFactor":18,"impactFactorByYear":18,"i10Index":136,"i10IndexLast5Year":136,"totalPublication":662,"totalPublicationByYear":663,"totalCitation":662,"totalCitationByYear":664,"totalCitationPerPublication":190,"totalCitationPerPublicationByYear":667,"hindexLast5Year":199,"hindex":199},476,{"0":349,"2019":136,"2021":286,"2022":595,"2023":104,"2024":495,"2025":199,"2026":198},{"2021":192,"2022":136,"2023":306,"2024":665,"2025":498,"2026":666},136,83,{"2021":254,"2022":649,"2023":668,"2024":274,"2025":669,"2026":144},0.62,25.43,{"id":671,"createTime":672,"updateTime":520,"relativeEntities":673,"slug":674,"properties":675,"entityType":16,"verifyStatus":178,"verifyTime":18,"verifyNote":18,"languages":687,"translateLanguages":18,"viewCount":280,"subjectFields":688,"manageAffiliations":689,"indexDatabases":690,"url":691,"thumbnailPath":692,"statistic":693,"gsStatistic":728,"type":155,"analyzePriority":18},"6984a56a-db70-403b-9cc4-4013e1ceaffa","2023-05-09T06:47:40.346+00:00",[],"T%E1%BA%A1p%20ch%C3%AD%20Nghi%C3%AAn%20c%E1%BB%A9u%20n%C6%B0%E1%BB%9Bc%20ngo%C3%A0i",{"country":676,"issn":677,"title":679,"introduce":682,"gsId":685},{"VOID":168},{"VOID":678},"25252445",{"EN":680,"VI":681},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":683,"VI":684},"{\"ops\":[{\"insert\":\"\\n\\nThe \\n\"},{\"attributes\":{\"italic\":true},\"insert\":\"VNU Journal of Science\"},{\"insert\":\"\\n was established in 1985 for the publication of national and international research papers in all fields of natural sciences and technology, social sciences and humanities. Since then, the journal has grown in quality, size and scope and now comprises a dozen of serials spanning academic research. 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Although, the main text structure may vary based on the review subtopics, the articles should be formatted according to suitable Templates as research articles.\"},{\"attributes\":{\"align\":\"justify\"},\"insert\":\"\\n\"},{\"insert\":\"\\n\"}]}","{\"ops\":[{\"insert\":\"Tạp chí Khoa học Trường ĐHSP Hà Nội 2 nhằm mục đích cung cấp một nền tảng liên ngành của sự phổ biến những tiến bộ của khoa học và công nghệ. Tạp chí xuất bản các bài báo gốc có giá trị khoa học hoặc công nghệ trong tất cả các lĩnh vực khoa học tự nhiên, xã hội hoặc giáo dục.\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Chuyên san Khoa học tự nhiên và công nghệ:\"},{\"insert\":\" Là các bài báo mô tả những phát hiện có giá trị trong vật lý, toán học, hóa học, sinh học; giải quyết các vấn đề kỹ thuật hoặc công nghệ.\"},{\"attributes\":{\"list\":\"bullet\"},\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Chuyên san Khoa học Xã hội và Nhân văn:\"},{\"insert\":\" là các bài báo xuất bản chất lượng cao trong các lĩnh vực khác nhau của khoa học xã hội và nghiên cứu phát triển con người.\"},{\"attributes\":{\"list\":\"bullet\"},\"insert\":\"\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Chuyên san Khoa học giáo dục:\"},{\"insert\":\" là các bài báo xuất bản trong lĩnh vực khoa học giáo dục và các ứng dụng của tiến bộ vào giáo dục để cải thiện và nâng cao giáo dục khoa học ở tất cả các cấp.\"},{\"attributes\":{\"list\":\"bullet\"},\"insert\":\"\\n\"},{\"insert\":\"Tạp chí trường ĐHSP Hà Nội 2 xuất bản được phản biện kín, xét duyệt bởi ít nhất 02 chuyên gia, và được đánh giá, chọn lựa từ ban biên tập và Tổng biên tập.\\n\"},{\"attributes\":{\"bold\":true},\"insert\":\"Các loại bài báo\"},{\"insert\":\":\\nBài báo nghiên cứu:\"},{\"attributes\":{\"list\":\"ordered\"},\"insert\":\"\\n\"},{\"insert\":\"Báo cáo học thuật về nghiên cứu ban đầu chưa từng được xuất bản ở bất kỳ nơi nào, hay bằng bất kỳ ngôn ngữ nào khác. Bản thảo thích hợp, nên chứa các phần sau theo thứ tự: Tiêu đề, Tác giả, Liên kết tác giả, Địa chỉ email của tác giả tương ứng, Tóm tắt, Từ khóa, Danh pháp (nếu có), Giới thiệu, Thử nghiệm, Lý thuyết, Kết quả và thảo luận, Kết luận, Xung đột quan tâm, Lời cảm ơn (nếu có), Tài liệu tham khảo, Phụ lục (nếu có). Bản xuất bản trước phải được định dạng theo Mẫu (phiên bản MS-Word).\\n2. Bài báo tổng quan:\\nNgoài các bài phê bình được mời, các bài phê bình tài liệu, bài phê bình có hệ thống và bài phê bình sẽ được chấp nhận để xem xét. Bản thảo cần được soạn thảo và sắp xếp theo trình tự yêu cầu: Tên sách, Tên tác giả, Liên kết, Địa chỉ email, Tóm tắt, Từ khóa, Nội dung chính, Kết luận, Xung đột lợi ích, Lời cảm ơn (nếu có), Tài liệu tham khảo. Mặc dù, cấu trúc văn bản chính có thể thay đổi dựa trên các chủ đề phụ của bài đánh giá, các bài báo nên được định dạng theo các Mẫu phù hợp như các bài báo nghiên cứu.\\n\"}]}",{"VOID":856},"YPoBvsIAAAAJ",[],[],[],"https:\u002F\u002Fsj.hpu2.edu.vn\u002Findex.php\u002Fjournal","\u002Fapi\u002Fpublic\u002Ffile\u002Fpublisher\u002F954132b5-ca74-461c-b819-45ad6e49a404\u002F2790ef1d0a7d7a40a504c2fc1647f670.jpg",{"impactFactor":19,"impactFactorByYear":863,"i10Index":19,"i10IndexLast5Year":19,"totalPublication":469,"totalPublicationByYear":865,"totalCitation":281,"totalCitationByYear":866,"totalCitationPerPublication":660,"totalCitationPerPublicationByYear":867,"hindexLast5Year":136,"hindex":136},{"2024":864},0.17,{"2022":283,"2023":419,"2024":289},{"2022":495,"2023":273,"2024":136},{"2022":314,"2023":367,"2024":310},{"impactFactor":18,"impactFactorByYear":18,"i10Index":195,"i10IndexLast5Year":195,"totalPublication":470,"totalPublicationByYear":869,"totalCitation":300,"totalCitationByYear":870,"totalCitationPerPublication":871,"totalCitationPerPublicationByYear":872,"hindexLast5Year":196,"hindex":196},{"0":136,"2022":281,"2023":283,"2024":218,"2025":292},{"2023":196,"2024":283,"2025":345,"2026":419},1.22,{"2023":262,"2024":479,"2025":873},4.56,{"id":875,"createTime":876,"updateTime":877,"relativeEntities":878,"slug":879,"properties":880,"entityType":16,"verifyStatus":178,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":218,"subjectFields":892,"manageAffiliations":893,"indexDatabases":901,"url":941,"thumbnailPath":18,"statistic":942,"gsStatistic":972,"type":155,"analyzePriority":18},"21ccdb34-414d-420f-8a60-a592a2fa848e","2023-05-29T10:42:53.358+00:00","2026-08-27T01:57:29.560+00:00",[],"Vietnam-Journal-of-Earth-Sciences",{"country":881,"eissn":882,"issn":884,"title":886,"introduce":888,"gsId":890},{"VOID":168},{"VOID":883},"26159783",{"VOID":885},"08667187",{"EN":887},"Vietnam Journal of Earth Sciences",{"EN":889},"Science of the Earth, formerly Vietnam Journal of Earth Sciences, is a peer-reviewed journal to publish high-quality articles on the entire range of earth sciences and the environment, focused on the Asia Pacific region and their correlations and connections to the globe. The journal publishes fundamental and applied research in earth sciences and the environment, including geology, geophysics, geography, soil science, hydrology, meteorology, oceanography, petroleum, geohazards, environmental sciences, environmental engineering, sustainable development, geoinformatics, geodesy, GIS, and remote sensing.",{"VOID":891},"5htfr3YAAAAJ",[],[894],{"id":222,"createTime":18,"updateTime":18,"relativeEntities":895,"slug":18,"properties":896,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":231,"parentIds":900,"statistic":18},[],{"title":897,"country":898,"abbreviation":899},{"EN":226,"VI":227},{"VOID":168},{"VOID":230},[],[902,914,925],{"id":903,"indexDatabase":904,"url":909,"indexYears":910,"academicFieldIds":911,"indexDatabaseRanking":913},"6ace2085-a177-4a27-b309-8813b832111e",{"id":52,"createTime":18,"updateTime":18,"relativeEntities":905,"label":906,"description":907,"key":58,"publicationTags":908,"standard":18},[],{"EN":55,"VI":55},{"EN":55,"VI":57},[60],"https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F21101039869","2018-2024",[912],"1689391c-5702-4349-aaa7-d720ee4321fc","NONE",{"id":915,"indexDatabase":916,"url":921,"indexYears":922,"academicFieldIds":923,"indexDatabaseRanking":18},"dadb15a8-ee22-41c2-a287-49e969d9a998",{"id":237,"createTime":18,"updateTime":18,"relativeEntities":917,"label":918,"description":919,"key":243,"publicationTags":920,"standard":18},[],{"EN":240,"VI":240},{"EN":242,"VI":242},[245],"https:\u002F\u002Fasean-cites.org\u002Fjournal_info?jid=10629","2016-2022",[924],"e04f14cf-280b-4aa8-b711-b77ddd79cbaf",{"id":926,"indexDatabase":927,"url":938,"indexYears":18,"academicFieldIds":939,"indexDatabaseRanking":18},"06f278ee-37b9-41eb-a9b0-3d2d77fa502b",{"id":928,"createTime":18,"updateTime":18,"relativeEntities":929,"label":930,"description":932,"key":935,"publicationTags":936,"standard":18},"88bab0f7-443b-476c-a72a-7fa5222da393",[],{"EN":931,"VI":931},"ISI\u002FESCI  - 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However, there is still no direct evidence that MTA1 promotes NPC growth in vivo. In this study, we aimed to investigate the function of MTA1 in the regulation of NPC cell proliferation and tumorigenesis in vitro and in vivo. Stable MTA1 knockdown or overexpression NPC cell lines were employed. The effects of MTA1 depletion or overexpression on cell proliferation, colony formation, cell cycle progression were examined by MTT, colony formation and flow cytometry assay. The effects of MTA1 depletion on tumor growth in vivo were examined in mouse xenograft model. MTA1 knockdown or overexpression drastically changed the proliferation, colony formation and cell cycle of NPC cells in vitro. MTA1 depletion significantly suppressed NPC tumorigenesis in vivo. MTA1 promotes NPC cell proliferation via enhancing G1 to S phase transition, leading to increased tumor growth. Targeting MTA1 is a promising approach to reduce tumor burden of NPC.",{"EN":1001},"MTA1 promotes nasopharyngeal carcinoma growth in vitro and in vivo",{"VOID":1003},"Chen MK, Chen TH, Liu JP, Chang CC, Chie WC: Better prediction of prognosis for patients with nasopharyngeal carcinoma using primary tumor volume. Cancer. 2004, 100 (10): 2160-2166. 10.1002\u002Fcncr.20210.\nSze WM, Lee AW, Yau TK, Yeung RM, Lau KY, Leung SK, Hung AW, Lee MC, Chappell R, Chan K: Primary tumor volume of nasopharyngeal carcinoma: prognostic significance of local control. Int J Radiat Oncol Biol Phys. 2004, 59 (1): 21-27. 10.1016\u002Fj.ijrobp.2003.10.027.\nWu Z, Gu MF, Zeng RF, Su Y, Huang SM: Correlation between nasopharyngeal carcinoma tumor volume and the 2002 international union against cancer tumor classification system. Radiat Oncol. 2013, 8 (1): 87-10.1186\u002F1748-717X-8-87.\nGuo R, Sun Y, Yu XL, Yin WJ, Li WF, Chen YY, Mao YP, Liu LZ, Li L, Lin AH, Ma J: Is primary tumor volume still a prognostic factor in intensity modulated radiation therapy for nasopharyngeal carcinoma?. Radiother Oncol. 2012, 104 (3): 294-299. 10.1016\u002Fj.radonc.2012.09.001.\nToh Y, Nicolson GL: The role of the MTA family and their encoded proteins in human cancers: molecular functions and clinical implications. Clin Exp Metastasis. 2009, 26 (3): 215-227. 10.1007\u002Fs10585-008-9233-8.\nLi Y, Chao Y, Fang Y, Wang J, Wang M, Zhang H, Ying M, Zhu X, Wang H: MTA1 promotes the invasion and migration of non-small cell lung cancer cells by downregulating miR-125b. J Exp Clin Cancer Res. 2013, 32: 33-10.1186\u002F1756-9966-32-33.\nSong Q, Li Y, Zheng X, Fang Y, Chao Y, Yao K, Zhu X: MTA1 contributes to actin cytoskeleton reorganization and metastasis of nasopharyngeal carcinoma by modulating Rho GTPases and Hedgehog signaling. Int J Biochem Cell Biol. 2013, 45 (7): 1439-1446. 10.1016\u002Fj.biocel.2013.04.017.\nLi WF, Liu N, Cui RX, He QM, Chen M, Jiang N, Sun Y, Zeng J, Liu LZ, Ma J: Nuclear overexpression of metastasis-associated protein 1 correlates significantly with poor survival in nasopharyngeal carcinoma. J Transl Med. 2012, 10: 78-10.1186\u002F1479-5876-10-78.\nDeng YF, Zhou DN, Ye CS, Zeng L, Yin P: Aberrant expression levels of MTA1 and RECK in nasopharyngeal carcinoma: association with metastasis, recurrence, and prognosis. Ann Otol Rhinol Laryngol. 2012, 121 (7): 457-465.\nCaysa H, Hoffmann S, Luetzkendorf J, Mueller LP, Unverzagt S, Mäder K, Mueller T: Monitoring of xenograft tumor growth and response to chemotherapy by non-invasive in vivo multispectral fluorescence imaging. PLoS One. 2012, 7 (10): e47927-10.1371\u002Fjournal.pone.0047927.\nMoon WS, Chang K, Tarnawski AS: Overexpression of metastatic tumor antigen 1 in hepatocellular carcinoma: Relationship to vascular invasion and estrogen receptor-alpha. Hum Pathol. 2004, 35 (4): 424-429. 10.1016\u002Fj.humpath.2003.11.007.\nNawa A, Nishimori K, Lin P, Maki Y, Moue K, Sawada H, Toh Y, Fumitaka K, Nicolson GL: Tumor metastasis-associated human MTA1 gene: its deduced protein sequence, localization, and association with breast cancer cell proliferation using antisense phosphorothioate oligonucleotides. J Cell Biochem. 2000, 79 (2): 202-212. 10.1002\u002F1097-4644(20001101)79:2\u003C202::AID-JCB40>3.0.CO;2-L.\nMazumdar A, Wang RA, Mishra SK, Adam L, Bagheri-Yarmand R, Mandal M, Vadlamudi RK, Kumar R: Transcriptional repression of oestrogen receptor by metastasis-associated protein 1 corepressor. Nat Cell Biol. 2001, 3 (1): 30-37. 10.1038\u002F35050532.\nBagheri-Yarmand R, Talukder AH, Wang RA, Vadlamudi RK, Kumar R: Metastasis- associated protein 1 deregulation causes inappropriate mammary gland development and tumorigenesis. Development. 2004, 131 (14): 3469-3479. 10.1242\u002Fdev.01213.\nSingh RR, Kumar R: MTA family of transcriptional metaregulators in mammary gland morphogenesis and breast cancer. J Mammary Gland Biol Neoplasia. 2007, 12 (2–3): 115-125.\nMahoney MG, Simpson A, Jost M, Noé M, Kari C, Pepe D, Choi YW, Uitto J, Rodeck U: Metastasis-associated protein (MTA)1 enhances migration, invasion, and anchorage-independent survival of immortalized human keratinocytes. Oncogene. 2002, 21 (14): 2161-2170. 10.1038\u002Fsj.onc.1205277.\nZhu X, Zhang X, Wang H, Song Q, Zhang G, Yang L, Geng J, Li X, Yuan Y, Chen L: MTA1 gene silencing inhibits invasion and alters the microRNA expression profile of human lung cancer cells. Oncol Rep. 2012, 28 (1): 218-224.\nZheng C, Jia W, Tang Y, Zhao H, Jiang Y, Sun S: Mesothelin regulates growth and apoptosis in pancreatic cancer cells through p53-dependent and -independent signal pathway. J Exp Clin Cancer Res. 2012, 31: 84-10.1186\u002F1756-9966-31-84.\nMoon HE, Cheon H, Lee MS: Metastasis-associated protein 1 inhibits p53-induced apoptosis. Oncol Rep. 2007, 18 (5): 1311-1314.\nKai L, Samuel SK, Levenson AS: Resveratrol enhances p53 acetylation and apoptosis in prostate cancer by inhibiting MTA1\u002FNuRD complex. Int J Cancer. 2010, 126 (7): 1538-1548.\nLi DQ, Pakala SB, Reddy SD, Ohshiro K, Peng SH, Lian Y, Fu SW, Kumar R: Revelation of p53-independent function of MTA1 in DNA damage response via modulation of the p21 WAF1-proliferating cell nuclear antigen pathway. J Biol Chem. 2010, 285 (13): 10044-10052. 10.1074\u002Fjbc.M109.079095.",{"VOID":1005},"10.1186\u002F1756-9966-32-54","PUBLICATION","Auto Verify","https:\u002F\u002Fjeccr.biomedcentral.com\u002Farticles\u002F10.1186\u002F1756-9966-32-54",[1010,1026,1041,1054,1067,1080,1093,1106,1119],{"id":1011,"sortIndex":19,"researcher":18,"roles":1012,"affiliations":1014,"properties":1023,"displayName":1025,"givenName":18,"familyName":18},"3cbf93f7-0817-4cbd-bd15-5e7a9b50f8e8",[1013],"AUTHOR",[1015],{"id":1016,"sortIndex":19,"affiliation":1017,"properties":18},"cff35bcd-d46a-48e5-84cc-a4b816288ec8",{"id":1016,"createTime":18,"updateTime":18,"relativeEntities":1018,"slug":18,"properties":1019,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1022,"statistic":18},[],{"title":1020},{"VI":1021},"Cancer Research Institute, Key Lab for Transcriptomics and Proteomics of Human Fatal Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China",[],{"title":1024},{"VI":1025},"Qingcui Song",{"id":1027,"sortIndex":190,"researcher":18,"roles":1028,"affiliations":1029,"properties":1038,"displayName":1040,"givenName":18,"familyName":18},"e2e2d702-8324-43c7-b4fb-84022aab9683",[1013],[1030],{"id":1031,"sortIndex":19,"affiliation":1032,"properties":18},"5c7699d4-ca73-45a9-9b9d-12268337450a",{"id":1031,"createTime":18,"updateTime":18,"relativeEntities":1033,"slug":18,"properties":1034,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1037,"statistic":18},[],{"title":1035},{"VI":1036},"Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China",[],{"title":1039},{"VI":1040},"Hong Zhang",{"id":1042,"sortIndex":136,"researcher":18,"roles":1043,"affiliations":1044,"properties":1051,"displayName":1053,"givenName":18,"familyName":18},"e9c5ccf8-ed7f-4329-a1c6-472047fd3850",[1013],[1045],{"id":1031,"sortIndex":19,"affiliation":1046,"properties":18},{"id":1031,"createTime":18,"updateTime":18,"relativeEntities":1047,"slug":18,"properties":1048,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1050,"statistic":18},[],{"title":1049},{"VI":1036},[],{"title":1052},{"VI":1053},"Min Wang",{"id":1055,"sortIndex":192,"researcher":18,"roles":1056,"affiliations":1057,"properties":1064,"displayName":1066,"givenName":18,"familyName":18},"9386becd-22b4-46ec-b59a-7ab3586de14a",[1013],[1058],{"id":1031,"sortIndex":19,"affiliation":1059,"properties":18},{"id":1031,"createTime":18,"updateTime":18,"relativeEntities":1060,"slug":18,"properties":1061,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1063,"statistic":18},[],{"title":1062},{"VI":1036},[],{"title":1065},{"VI":1066},"Wen 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inhibitors (ICI) can lead to immune-related adverse events (irAEs) in a significant proportion of patients. The mechanisms underlying irAEs development are mostly unknown and might involve multiple immune effectors, such as T cells, B cells and autoantibodies (AutoAb). We used custom autoantigen (AutoAg) microarrays to profile AutoAb related to irAEs in patients receiving ICI. Plasma was collected before and after ICI from cancer patients participating in two clinical trials (NCT03686202, NCT02644369). A one-time collection was obtained from healthy controls for comparison. Custom arrays with 162 autoAg were used to detect IgG and IgM reactivities. Differences of median fluorescent intensity (MFI) were analyzed with Wilcoxon sign rank test and Kruskal–Wallis test. MFI 500 was used as threshold to define autoAb reactivity. A total of 114 patients and 14 healthy controls were included in this study. irAEs of grade (G) ≥ 2 occurred in 37\u002F114 patients (32%). We observed a greater number of IgG and IgM reactivities in pre-ICI collections from patients versus healthy controls (62 vs 32 p \u003C 0.001). Patients experiencing irAEs G ≥ 2 demonstrated pre-ICI IgG reactivity to a greater number of AutoAg than patients who did not develop irAEs (39 vs 33 p = 0.040). We observed post-treatment increase of IgM reactivities in subjects experiencing irAEs G ≥ 2 (29 vs 35, p = 0.021) and a decrease of IgG levels after steroids (38 vs 28, p = 0.009). Overall, these results support the potential role of autoAb in irAEs etiology and evolution. A prospective study is ongoing to validate our findings (NCT04107311).",{"EN":1198},"Autoimmune PaneLs as PrEdictors of Toxicity in Patients TReated with Immune Checkpoint InhibiTors (ALERT)",{"VOID":1200},"Akinleye A, Rasool Z. Immune checkpoint inhibitors of PD-L1 as cancer therapeutics. 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Their formalin-fixed, paraffin-embedded tissue specimens were immunohistochemically stained for Tau protein, using semi-quantitative DAKO test. Tau expression was acknowledged as negative (0 and 1+) or positive (2+ and 3+). The correlation between Tau expression, progression free survival (PFS) and overall survival (OS) was evaluated. Statistical analysis included Kaplan-Meyer estimator, long rank test, Mann Whitney test and Cox proportional hazards model. 25.7% (19\u002F74) and 74.3% (55\u002F74) of the patients were classified as Tau-negative and Tau-positive, respectively. Median PFS was 28.7 months for Tau-negative group and 15.9 months for Tau-positive group (p = 0.0355). In the univariate analysis 3-year OS in Tau-negative and Tau-positive groups was 80.2% and 52.4%, respectively (p = 0.0198). Low expression of protein Tau was associated with better OS, whereas an advanced stage at diagnosis, suboptimal surgery, serous histological type and resistance to first line chemotherapy were each correlated with worse OS (p \u003C0,05). In multivariate analysis only resistance to first line chemotherapy remained significant (HR 22.59; 95% CI, 8.71-58.55; p \u003C0.0001). Negative tau protein seems to be both good prognostic factor and a predictor of response to paclitaxel\u002Fplatinum-based chemotherapy in EOC patients.",{"EN":1552},"Tau protein as a potential predictive marker in epithelial ovarian cancer patients treated with paclitaxel\u002Fplatinum first-line chemotherapy",{"VOID":1554},"McGuire WP, Hoskins WJ, Brady MF: Cyclophosphamide and cisplatin compared with paclitaxel and cisplatin in patients with stage III and stage IV ovarian cancer. N Engl J Med. 1996, 334: 1-6. 10.1056\u002FNEJM199601043340101.\nPiccart M, Bertrlsen K, James K: Randomized intergroup trial of cisplatin- paclitaxel versus cisplatin- cyclophosphamide in women with advanced epithelial ovarian cancer: three year results. J Natl Cancer Inst. 2000, 92: 699-708. 10.1093\u002Fjnci\u002F92.9.699.\nAmos LA, Löwe J: How Taxol stabilises microtubule structure. Chem Biol. 1999, 6: 65-9. 10.1016\u002FS1074-5521(99)89002-4.\nRouzier R, Rajan R, Wagner P: Microtubule-associated protein tau: a marker of paclitaxel sensitivity in breast cancer. Proc Natl Acad Sci USA. 2005, 102: 8315-20. 10.1073\u002Fpnas.0408974102.\nKar S, Fan J, Smith MJ, Goedert M, Amos LA: Repeat motifs of tau bind to the insides of microtubules in the absence of taxol. EMBO J. 2003, 22: 70-77. 10.1093\u002Femboj\u002Fcdg001.\nDye RB, Fink SP, Williams RC: Taxol- induced Flexibility of Microtubules and Its reversal by MAP-2 and Tau. J Biol Chem. 1993, 268: 6847-6850.\nRobert M, Mathuranath PS: Tau and taupathies. Neurol India. 2007, 55: 11-16. 10.4103\u002F0028-3886.30420.\nPusztai L, Jeong JH, Gong Y: Evaluation of microtubule-associated protein-Tau expression as a prognostic and predictive marker in the NSABP-B 28 randomized clinical trial. J Clin Oncol. 2009, 27: 4287-92. 10.1200\u002FJCO.2008.21.6887.\nMimori K, Sadanaga N, Yoshikawa Y: Reduced tau expression in gastric cancer can identify candidates for successful Paclitaxel treatment. Br J Cancer. 2006, 94: 1894-7. 10.1038\u002Fsj.bjc.6603182.\nTanaka S, Nohara T, Iwamoto M: Tau expression and efficacy of paclitaxel treatment in metastatic breast cancer. Cancer Chemother Pharmacol. 2009, 64: 341-6. 10.1007\u002Fs00280-008-0877-5.\nPentheroudakis G, Kalogeras KT, Wirtz RM: Gene expression of estrogen receptor, progesterone receptor and microtubule-associated protein Tau in high-risk early breast cancer: a quest for molecular predictors of treatment benefit in the context of a Hellenic Cooperative Oncology Group trial. Breast Cancer Res Treat. 2009, 116: 131-43. 10.1007\u002Fs10549-008-0144-9.\nRody A, Karn T, Gätje R: Gene expression profiling of breast cancer patients treated with docetaxel, doxorubicin, and cyclophosphamide within the GEPARTRIO trial: HER-2, but not topoisomerase II alpha and microtubule-associated protein tau, is highly predictive of tumor response. Breast. 2007, 16: 86-93. 10.1016\u002Fj.breast.2006.06.008.\nGogas H, Pectasides D, Kostopoulos I: Paclitaxel and carboplatin as neoadjuvant chemotherapy in patients with locally advanced breast cancer: a phase II trial of the Hellenic cooperative oncology group. Clin Breast Cancer. 2010, 10: 230-7. 10.3816\u002FCBC.2010.n.031.\nFekete T, Rásó E, Pete I: Meta-analysis of gene expression profiles associated with histological classification and survival in 829 ovarian cancer samples. Int J Cancer. 2012, 131: 95-105. 10.1002\u002Fijc.26364.\nShao YY, Kuo KT, Hu FC: Predictive and prognostic values of tau and ERCC1 in advanced breast cancer patients treated with paclitaxel and cisplatin. Jpn J Clin Oncol. 2010, 40: 286-93. 10.1093\u002Fjjco\u002Fhyp184.\nHan LY, Karavasilis V, Hagen T: Doubling time of serum CA125 is an independent prognostic factor for survival in patients with ovarian cancer relapsing after first-line chemotherapy. Eur J Cancer. 2010, 46: 1359-64. 10.1016\u002Fj.ejca.2010.02.012.\nBae J, Lim MC, Choi JH: Prognostic factors of secondary cytoreductive surgery for patients with recurrent epithelial ovarian cancer. 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carcinoma (HCC), a major cause of cancer death in China, is preceded by chronic hepatitis and liver cirrhosis (LC). Although hepatitis B virus (HBV) has been regarded as a clear etiology of human hepatocarcinogenesis, the mechanism is still needs to be further clarified. In this study, we used a proteomic approach to identify the differential expression protein profiles between HCC and the adjacent non-tumorous liver tissues. Eighteen cases of HBV-related HCC including 12 cases of LC-developed HCC and 6 cases of chronic hepatitis B (CHB)-developed HCC were analyzed by two-dimensional electrophoresis (2-DE) combined with matrix-assisted laser desorption\u002Fionization time of flight mass spectrometry (MALDI-TOF-MS), and the results were compared to those of paired adjacent non-tumorous liver tissues. A total of 17 differentially expressed proteins with diverse biological functions were identified. Among these, 10 proteins were up-regulated, whereas the other 7 proteins were down-regulated in cancerous tissues. Two proteins, c-Jun N-terminal kinase 2 and ADP\u002FATP carrier protein were found to be up-regulated only in CHB-developed HCC tissues. Insulin-like growth factor binding protein 2 and Rho-GTPase-activating protein 4 were down-regulated in LC-developed and CHB-developed HCC tissues, respectively. Although 11 out of these 17 proteins have been already described by previous studies, or are already known to be involved in hepatocarcinogenesis, this study revealed 6 new proteins differentially expressed in HBV-related HCC. These findings elucidate that there are common features between CHB-developed HCC and LC-developed HCC. The identified proteins are valuable for studying the hepatocarcinogenesis, and may be potential diagnostic markers or therapeutic targets for HBV-related HCC.",{"EN":1716},"Proteomic analysis of differentially expressed proteins in hepatitis B virus-related hepatocellular carcinoma tissues",{"EN":1718},"",{"VOID":1720},"Park NH, Song IH, Chung YH: Chronic hepatitis B in hepatocarcinogenesis. Postgrad Med J. 2006, 82 (970): 507-515. 10.1136\u002Fpgmj.2006.047431.\nXie H, Song J, Du R, Liu K, Wang J, Tang H, Bai F, Liang J, Lin T, Liu J, Fan D: Prognostic significance of osteopontin in hepatitis B virus-related hepatocellular carcinoma. Dig Liver Dis. 2007, 39 (2): 167-172. 10.1016\u002Fj.dld.2006.10.015.\nFeng JT, Shang S, Beretta L: Proteomics for the early detection and treatment of hepatocellular carcinoma. Oncogene. 2006, 25 (27): 3810-3817. 10.1038\u002Fsj.onc.1209551.\nBruix J, Sherman M, Llovet JM, Beaugrand M, Lencioni R, Burroughs AK, Christensen E, Pagliaro L, Colombo M, Rodés J, EASL Panel of Experts on HCC: Clinical management of hepatocellular carcinoma. Conclusions of the Barcelona-2000 EASL conference. European Association for the Study of the Liver. J Hepatol. 2001, 35 (3): 421-430. 10.1016\u002FS0168-8278(01)00130-1.\nBlanc JF, Lalanne C, Plomion C, Schmitter JM, Bathany K, Gion JM, Bioulac-Sage P, Balabaud C, Bonneu M, Rosenbaum J: Proteomic analysis of differentially expressed proteins in hepatocellular carcinoma developed in patients with chronic viral hepatitis C. Proteomics. 2005, 5 (14): 3778-3789. 10.1002\u002Fpmic.200401194.\nLi C, Xiao Z, Chen Z, Zhang X, Li J, Wu X, Li X, Yi H, Li M, Zhu G, Liang S: Proteome analysis of human lung squamous carcinoma. Proteomics. 2006, 6 (2): 547-558. 10.1002\u002Fpmic.200500256.\nLi M, Xiao ZQ, Chen ZC, Li JL, Li C, Zhang PF, Li MY: Proteomic analysis of the aging-related proteins in human normal colon epithelial tissue. J Biochem Mol Biol. 2007, 40 (1): 72-81.\nCheng AL, Huang WG, Chen ZC, Peng F, Zhang PF, Li MY, Li F, Li JL, Li C, Yi H, Yi B, Xiao ZQ: Identification of novel nasopharyngeal carcinoma biomarkers by laser capture microdissection and proteomic analysis. Clin Cancer Res. 2008, 14 (2): 435-445. 10.1158\u002F1078-0432.CCR-07-1215.\nBergsland EK: Molecular mechanisms underlying the development of hepatocellular carcinoma. Semin Oncol. 2001, 28 (5): 521-531. 10.1016\u002FS0093-7754(01)90145-9.\nLok AS, Heathcote EJ, Hoofnagle JH: Management of hepatitis B: 2000 – summary of a workshop. Gastroenterology. 2001, 120 (7): 1828-1853. 10.1053\u002Fgast.2001.24839.\nHuang YJ, Xuan C, Zhang BB, Liao M, Deng KF, He M, Zhao JM: SELDI-TOF MS profiling of serum for detection of nasopharyngeal carcinoma. J Exp Clin Cancer Res. 2009, 28: 85-10.1186\u002F1756-9966-28-85.\nLee NP, Chen L, Lin MC, Tsang FH, Yeung C, Poon RT, Peng J, Leng X, Beretta L, Sun S, Day PJ, Luk JM: Proteomic expression signature distinguishes cancerous and nonmalignant tissues in hepatocellular carcinoma. J Proteome Res. 2009, 8 (3): 1293-303. 10.1021\u002Fpr800637z.\nZinkin NT, Grall F, Bhaskar K, Otu HH, Spentzos D, Kalmowitz B, Wells M, Guerrero M, Asara JM, Libermann TA, Afdhal NH: Serum proteomics and biomarkers in hepatocellular carcinoma and chronic liver disease. Clin Cancer Res. 2008, 14 (7): 470-477. 10.1158\u002F1078-0432.CCR-07-0586.\nTugendreich S, Tomkiel J, Earnshaw W, Hieter P: CDC27Hs colocalizes with CDC16Hs to the centrosome and mitotic spindle and is essential for the metaphase to anaphase transition. Cell. 1995, 81 (2): 261-268. 10.1016\u002F0092-8674(95)90336-4.\nFan CW, Chan CC, Chao CC, Fan HA, Sheu DL, Chan EC: Expression patterns of cell cycle and apoptosis-related genes in a multidrug-resistant human colon carcinoma cell line. Scand J Gastroenterol. 2004, 39 (5): 464-469. 10.1080\u002F00365520310008809.\nWhyte L, Huang YY, Torres K, Mehta RG: Molecular mechanisms of resveratrol action in lung cancer cells using dual protein and microarray analyses. Cancer Res. 2007, 67 (24): 12007-12017. 10.1158\u002F0008-5472.CAN-07-2464.\nKato M, Yamashina S, Takeda N, Mochizuki S, Morishita T, Nagano M: Molecular biological and quantitative abnormalities of ADP\u002FATP carrier protein in cardiomyopathic hamsters. Eur Heart J. 1995, 16 (Suppl O): 78-80.\nSchulze K, Schultheiss HP: The role of the ADP\u002FATP carrier in the pathogenesis of viral heart disease. Eur Heart J. 1995, 16 (Suppl O): 64-67.\nLeirdal M, Shadidy M, Røsok Ø, Sioud M: Identification of genes differentially expressed in breast cancer cell line SKBR3: potential identification of new prognostic biomarkers. Int J Mol Med. 2004, 14 (2): 217-222.\nVogt DL, Gray CD, Young WS, Orellana SA, Malouf AT: ARHGAP4 is a novel RhoGAP that mediates inhibition of cell motility and axon outgrowth. Mol Cell Neurosci. 2007, 36 (3): 332-342. 10.1016\u002Fj.mcn.2007.07.004.\nNagaraja GM, Kandpal RP: Chromosome 13q12 encoded Rho GTPase activating protein suppresses growth of breast carcinoma cells, and yeast two-hybrid screen shows its interaction with several proteins. Biochem Biophys Res Commun. 2004, 313 (3): 654-665. 10.1016\u002Fj.bbrc.2003.12.001.\nUllmannova V, Popescu NC: Inhibition of cell proliferation, induction of apoptosis, reactivation of DLC1, and modulation of other gene expression by dietary flavone in breast cancer cell lines. Cancer Detect Prev. 2007, 31 (2): 110-118. 10.1016\u002Fj.cdp.2007.02.005.\nWong CM, Yam JW, Ching YP, Yau TO, Leung TH, Jin DY, Ng IO: Rho GTPase-activating protein deleted in liver cancer suppresses cell proliferation and invasion in hepatocellular carcinoma. Cancer Res. 2005, 65 (19): 8861-8868. 10.1158\u002F0008-5472.CAN-05-1318.\nFatma N, Singh DP, Shinohara T, Chylack LT: Transcriptional Regulation of the Antioxidant Protein 2Gene, a Thiol-specific Antioxidant, by Lens Epithelium-derived Growth Factor to Protect Cells from Oxidative Stress. J Biol Chem. 2001, 276 (52): 48899-48907. 10.1074\u002Fjbc.M100733200.\nKubo E, Urakami T, Fatma N, Akagi Y, Singh DP: Polyol pathway-dependent osmotic and oxidative stresses in aldose reductase-mediated apoptosis in human lens epithelial cells: role of AOP2. Biochem Biophys Res Commun. 2004, 314 (4): 1050-1056. 10.1016\u002Fj.bbrc.2004.01.002.\nVáli L, Hahn O, Kupcsulik P, Drahos A, Sárváry E, Szentmihályi K, Pallai Z, Kurucz T, Sípos P, Blázovics A: Oxidative stress with altered element content and decreased ATP level of erythrocytes in hepatocellular carcinoma and colorectal liver metastases. Eur J Gastroenterol Hepatol. 2008, 20 (5): 393-398. 10.1097\u002FMEG.0b013e3282f495c7.\nTanaka H, Fujita N, Sugimoto R, Urawa N, Horiike S, Kobayashi Y, Iwasa M, Ma N, Kawanishi S, Watanabe S, Kaito M, Takei Y: Hepatic oxidative DNA damage is associated with increased risk for hepatocellular carcinoma in chronic hepatitis C. Br J Cancer. 2008, 98 (3): 580-586. 10.1038\u002Fsj.bjc.6604204.\nKuramitsu Y, Nakamura K: Proteomic analysis of cancer tissues: Shedding light on carcinogenesis and possible biomarkers. Proteomics. 2006, 6 (20): 5650-5661. 10.1002\u002Fpmic.200600218.\nEzzikouri S, El Feydi AE, Chafik A, Afifi R, El Kihal L, Benazzouz M, Hassar M, Pineau P, Benjelloun S: Genetic polymorphism in the manganese superoxide dismutase gene is associated with an increased risk for hepatocellular carcinoma in HCV-infected Moroccan patients. Mutat Res. 2008, 649 (1–2): 1-6.\nKuruma H, Egawa S, Oh-Ishi M, Kodera Y, Satoh M, Chen W, Okusa H, Matsumoto K, Maeda T, Baba S: High molecular mass proteome of androgen-independent prostate cancer. Proteomics. 2005, 5 (4): 1097-1112. 10.1002\u002Fpmic.200401115.\nTan S, Seow TK, Liang RC, Koh S, Lee CP, Chung MC, Hooi SC: Proteome analysis of butyrate-treated human colon cancer cells (HT-29). Int J Cancer. 2002, 98 (4): 523-531. 10.1002\u002Fijc.10236.\nPrasannan P, Pike S, Peng K, Shane B, Appling DR: Human mitochondrial C1-tetrahydrofolate synthase: gene structure, tissue distribution of the mRNA, and immunolocalization in Chinese hamster ovary calls. J Biol Chem. 2003, 278 (44): 43178-43187. 10.1074\u002Fjbc.M304319200.\nHoward KM, Muga SJ, Zhang L, Thigpen AE, Appling DR: Characterization of the rat cytoplasmic C1-tetrahydrofolate synthase gene and analysis of its expression in liver regeneration and fetal development. Gene. 2003, 319: 85-97. 10.1016\u002FS0378-1119(03)00796-0.",{"VOID":1722},"10.1186\u002F1756-9966-28-122","https:\u002F\u002Fjeccr.biomedcentral.com\u002Farticles\u002F10.1186\u002F1756-9966-28-122",[1725,1740,1755,1770,1783,1798,1813],{"id":1726,"sortIndex":19,"researcher":18,"roles":1727,"affiliations":1728,"properties":1737,"displayName":1739,"givenName":18,"familyName":18},"5d740b2f-65b6-44ea-9d77-442cc33cf2df",[1013],[1729],{"id":1730,"sortIndex":19,"affiliation":1731,"properties":18},"b7b589a9-95cd-4dad-93ed-e0c8fa912247",{"id":1730,"createTime":18,"updateTime":18,"relativeEntities":1732,"slug":18,"properties":1733,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1736,"statistic":18},[],{"title":1734},{"VI":1735},"Department of Blood transfusion, Xiangya Hospital, Central South University, Changsha, PR China",[],{"title":1738},{"VI":1739},"Ning Li",{"id":1741,"sortIndex":190,"researcher":18,"roles":1742,"affiliations":1743,"properties":1752,"displayName":1754,"givenName":18,"familyName":18},"823bf74b-42de-4d56-82d9-85a1e17a185b",[1013],[1744],{"id":1745,"sortIndex":19,"affiliation":1746,"properties":18},"504b858d-2c87-4951-a114-c7f41f3c6dd1",{"id":1745,"createTime":18,"updateTime":18,"relativeEntities":1747,"slug":18,"properties":1748,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1751,"statistic":18},[],{"title":1749},{"VI":1750},"Department of Infectious Diseases, the First Hospital of Zhuzhou, Zhuzhou, PR China",[],{"title":1753},{"VI":1754},"Yunzhu Long",{"id":1756,"sortIndex":136,"researcher":18,"roles":1757,"affiliations":1758,"properties":1767,"displayName":1769,"givenName":18,"familyName":18},"7965ca13-c7a6-4a2d-b834-41ff3df47f9a",[1013],[1759],{"id":1760,"sortIndex":19,"affiliation":1761,"properties":18},"d6727bdf-b28e-489a-9b3b-f627a4c1a9b7",{"id":1760,"createTime":18,"updateTime":18,"relativeEntities":1762,"slug":18,"properties":1763,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1766,"statistic":18},[],{"title":1764},{"VI":1765},"Department of Infectious Diseases, Xiangya Hospital, Central South University, Changsha, PR China",[],{"title":1768},{"VI":1769},"Xuegong Fan",{"id":1771,"sortIndex":192,"researcher":18,"roles":1772,"affiliations":1773,"properties":1780,"displayName":1782,"givenName":18,"familyName":18},"0a1f0c88-ce35-4e83-b200-f1a2f3105692",[1013],[1774],{"id":1760,"sortIndex":19,"affiliation":1775,"properties":18},{"id":1760,"createTime":18,"updateTime":18,"relativeEntities":1776,"slug":18,"properties":1777,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1779,"statistic":18},[],{"title":1778},{"VI":1765},[],{"title":1781},{"VI":1782},"Hongbo 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Chen",{"id":1814,"sortIndex":198,"researcher":18,"roles":1815,"affiliations":1816,"properties":1825,"displayName":1827,"givenName":18,"familyName":18},"695c400a-0cda-4e6a-9e12-4b7dbe116771",[1013],[1817],{"id":1818,"sortIndex":19,"affiliation":1819,"properties":18},"0356cbdb-4440-4745-9931-8a78dc45f9bc",{"id":1818,"createTime":18,"updateTime":18,"relativeEntities":1820,"slug":18,"properties":1821,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1824,"statistic":18},[],{"title":1822},{"VI":1823},"Department of Surgery, Xiangya Hospital, Central South University, Changsha, PR China",[],{"title":1826},{"VI":1827},"Zhiming Wang",{"url":18,"publisher":1829,"properties":18},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1830,"slug":10,"properties":1831,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1834,"manageAffiliations":1843,"indexDatabases":1854,"url":84,"thumbnailPath":18,"statistic":1869,"gsStatistic":18,"type":155,"analyzePriority":18},[],{"issn":1832,"title":1833},{"VOID":13},{"EN":15},[1835,1839],{"id":22,"createTime":18,"updateTime":18,"relativeEntities":1836,"label":1837,"description":1838,"parentId":18,"standard":18,"scholarHubFieldId":18},[],{"EN":25},{},{"id":28,"createTime":18,"updateTime":18,"relativeEntities":1840,"label":1841,"description":1842,"parentId":18,"standard":18,"scholarHubFieldId":18},[],{"EN":31},{},[1844,1849],{"id":35,"createTime":18,"updateTime":18,"relativeEntities":1845,"slug":18,"properties":1846,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1848,"statistic":18},[],{"title":1847},{"EN":39},[],{"id":42,"createTime":18,"updateTime":18,"relativeEntities":1850,"slug":18,"properties":1851,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1853,"statistic":18},[],{"title":1852},{"EN":46},[],[1855,1862],{"id":50,"indexDatabase":1856,"url":61,"indexYears":62,"academicFieldIds":1861,"indexDatabaseRanking":66},{"id":52,"createTime":18,"updateTime":18,"relativeEntities":1857,"label":1858,"description":1859,"key":58,"publicationTags":1860,"standard":18},[],{"EN":55,"VI":55},{"EN":55,"VI":57},[60],[64,65],{"id":68,"indexDatabase":1863,"url":81,"indexYears":18,"academicFieldIds":1868,"indexDatabaseRanking":18},{"id":70,"createTime":18,"updateTime":18,"relativeEntities":1864,"label":1865,"description":1866,"key":77,"publicationTags":1867,"standard":18},[],{"EN":73,"VI":73},{"EN":75,"VI":76},[79,80],[83],{"impactFactor":19,"impactFactorByYear":1870,"i10Index":99,"i10IndexLast5Year":100,"totalPublication":101,"totalPublicationByYear":1871,"totalCitation":119,"totalCitationByYear":1872,"totalCitationPerPublication":137,"totalCitationPerPublicationByYear":1873,"hindexLast5Year":154,"hindex":154},{"2012":87,"2013":88,"2014":89,"2015":90,"2016":91,"2017":92,"2018":93,"2019":94,"2020":95,"2021":96,"2022":97,"2023":98},{"2008":103,"2009":104,"2010":105,"2011":106,"2012":107,"2013":108,"2014":109,"2015":104,"2016":110,"2017":111,"2018":112,"2019":113,"2020":114,"2021":115,"2022":116,"2023":117,"2024":118},{"2008":121,"2009":122,"2010":123,"2011":124,"2012":125,"2013":126,"2014":127,"2015":128,"2016":129,"2017":130,"2018":131,"2019":132,"2020":133,"2021":134,"2022":135,"2024":136},{"2008":96,"2009":139,"2010":140,"2011":141,"2012":142,"2013":143,"2014":144,"2015":145,"2016":146,"2017":147,"2018":148,"2019":149,"2020":150,"2021":151,"2022":152,"2024":153},"2009-08-28",2009,[66,79],{"id":1878,"createTime":1879,"updateTime":1880,"relativeEntities":1881,"slug":1882,"properties":1883,"entityType":1006,"verifyStatus":178,"verifyTime":1880,"verifyNote":1007,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1892,"fullTextUrl":18,"authors":1893,"publicationType":1132,"publisherRelationship":1985,"citationCount":18,"citationInfo":18,"publishDate":2036,"publishYear":2037,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":2038,"openAccess":18,"references":18,"isForceReanalyzing":1187},"00c43fdd-9bbd-448f-8e5d-87e2b32e9b7e","2024-01-15T01:13:50.998+00:00","2024-12-24T00:22:22.482+00:00",[],"MicroRNA-based-theranostics-for-brain-cancer-basic-principles",{"abstract":1884,"title":1886,"references":1888,"doi":1890},{"EN":1885},"Because of the complexity of the blood-brain barrier (BBB), brain tumors, especially the most common and aggressive primary malignant tumor type arising from the central nervous system (CNS), glioblastoma, remain an essential challenge regarding diagnostic and treatment. There are no approved circulating diagnostic or prognostic biomarkers, nor novel therapies like immune checkpoint inhibitors for glioblastoma, and chemotherapy brings only minimal survival benefits. The development of molecular biology led to the discovery of new potential diagnostic tools and therapeutic targets, offering the premise to detect patients at earlier stages and overcome the current poor prognosis. One potential diagnostic and therapeutic breakthrough might come from microRNAs (miRNAs). It is well-known that miRNAs play a role in the initiation and development of various types of cancer, including glioblastoma. The review aims to answer the following questions concerning the role of RNA theranostics for brain tumors: (1) which miRNAs are the best candidates to become early diagnostic and prognostic circulating biomarkers?; (2) how to deliver the therapeutic agents in the CNS to overcome the BBB?; (3) which are the best methods to restore\u002Finhibit miRNAs? Because of the proven roles played by miRNAs in gliomagenesis and of their capacity to pass from the CNS tissue into the blood or cerebrospinal fluid (CSF), we propose miRNAs as ideal diagnostic and prognostic biomarkers. Moreover, recent advances in direct miRNA restoration (miRNA mimics) and miRNA inhibition therapy (antisense oligonucleotides, antagomirs, locked nucleic acid anti-miRNA, small molecule miRNA inhibitors) make miRNAs perfect candidates for entering clinical trials for glioblastoma treatment.",{"EN":1887},"MicroRNA based theranostics for brain cancer: basic principles",{"VOID":1889},"Ostrom QT, Gittleman H, Liao P, Vecchione-Koval T, Wolinsky Y, Kruchko C, et al. CBTRUS Statistical Report: Primary brain and other central nervous system tumors diagnosed in the United States in 2010–2014. Neuro Oncol. 2017;19(suppl_5):v1–v88.\nClaus EB, Walsh KM, Wiencke JK, Molinaro AM, Wiemels JL, Schildkraut JM, et al. 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Serum exosomal miR-301a as a potential diagnostic and prognostic biomarker for human glioma. Cell Oncol (Dordr). 2018;41(1):25–33.\nWu J, Li L, Jiang C. Identification and evaluation of serum MicroRNA-29 family for glioma screening. Mol Neurobiol. 2015;52(3):1540–6.\nChen J, Yang L, Wang X. Reduced circulating microRNA-203 predicts poor prognosis for glioblastoma. Cancer Biomark. 2017;20(4):521–6.\nLi HY, Li YM, Li Y, Shi XW, Chen H. Circulating microRNA-137 is a potential biomarker for human glioblastoma. Eur Rev Med Pharmacol Sci. 2016;20(17):3599–604.\nLai NS, Wu DG, Fang XG, Lin YC, Chen SS, Li ZB, et al. Serum microRNA-210 as a potential noninvasive biomarker for the diagnosis and prognosis of glioma. Br J Cancer. 2015;112(7):1241–6.\nZhang R, Pang B, Xin T, Guo H, Xing Y, Xu S, et al. Plasma miR-221\u002F222 family as novel descriptive and prognostic biomarkers for glioma. Mol Neurobiol. 2016;53(3):1452–60.\nWei X, Chen D, Lv T, Li G, Qu S. 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Identification of seven serum microRNAs from a genome-wide serum microRNA expression profile as potential noninvasive biomarkers for malignant astrocytomas. Int J Cancer. 2013;132(1):116–27.\nZhi F, Shao N, Wang R, Deng D, Xue L, Wang Q, et al. Identification of 9 serum microRNAs as potential noninvasive biomarkers of human astrocytoma. Neuro Oncol. 2015;17(3):383–91.\nGoze C, Reynes C, Forestier L, Sabatier R, Duffau H. Pilot study of whole blood MicroRNAs as potential tools for diffuse low-grade gliomas detection. Cell Mol Neurobiol. 2018;38(3):715–25.\nBaraniskin A, Kuhnhenn J, Schlegel U, Maghnouj A, Zollner H, Schmiegel W, et al. Identification of microRNAs in the cerebrospinal fluid as biomarker for the diagnosis of glioma. Neuro Oncol. 2012;14(1):29–33.\nAkers JC, Ramakrishnan V, Kim R, Skog J, Nakano I, Pingle S, et al. miR-21 in the Extracellular Vesicles (EVs) of Cerebrospinal Fluid (CSF): A Platform for Glioblastoma Biomarker Development. 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Genome Res. 2009;19(1):92–105.\nVasilescu C, Tanase M, Dragomir M, Calin GA. From mobility to crosstalk. A model of intracellular miRNAs motion may explain the RNAs interaction mechanism on the basis of target subcellular localization. Math Biosci. 2016;280:50–61.\nDragomir M, Mafra ACP, Dias SMG, Vasilescu C, Calin GA. Using microRNA Networks to Understand Cancer. Int J Mol Sci. 2018;19(7):1871.\nVolinia S, Galasso M, Costinean S, Tagliavini L, Gamberoni G, Drusco A, et al. Reprogramming of miRNA networks in cancer and leukemia. Genome Res. 2010;20(5):589–99.\nShankar GM, Balaj L, Stott SL, Nahed B, Carter BS. Liquid biopsy for brain tumors. Expert Rev Mol Diagn. 2017;17(10):943–7.\nBettegowda C, Sausen M, Leary RJ, Kinde I, Wang Y, Agrawal N, et al. Detection of circulating tumor DNA in early- and late-stage human malignancies. Sci Transl Med. 2014;6(224):224ra24.\nPan C, Diplas BH, Chen X, Wu Y, Xiao X, Jiang L, et al. Molecular profiling of tumors of the brainstem by sequencing of CSF-derived circulating tumor DNA. Acta Neuropathol. 2019;137(2):297–306.\nVecera M, Sana J, Lipina R, Smrcka M, Slaby O. Long non-coding RNAs in gliomas: from molecular pathology to diagnostic biomarkers and therapeutic targets. Int J Mol Sci. 2018;19(9):2754.\nZhang Y, Liang W, Zhang P, Chen J, Qian H, Zhang X, et al. Circular RNAs: emerging cancer biomarkers and targets. J Exp Clin Cancer Res. 2017;36(1):152.\nHao Z, Hu S, Liu Z, Song W, Zhao Y, Li M. Circular RNAs: Functions and Prospects in Glioma. J Mol Neurosci. 2019;67(1):72–81.\nWitwer KW. Circulating microRNA biomarker studies: pitfalls and potential solutions. Clin Chem. 2015;61(1):56–63.",{"VOID":1891},"10.1186\u002Fs13046-019-1180-5","https:\u002F\u002Fjeccr.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13046-019-1180-5",[1894,1918,1933,1948,1972],{"id":1895,"sortIndex":19,"researcher":18,"roles":1896,"affiliations":1897,"properties":1915,"displayName":1917,"givenName":18,"familyName":18},"630afaf8-981a-418f-9418-08eb4d800126",[1013],[1898,1906],{"id":1899,"sortIndex":19,"affiliation":1900,"properties":18},"7e7c818e-062c-4957-bfb6-5a9e88c073c8",{"id":1899,"createTime":18,"updateTime":18,"relativeEntities":1901,"slug":18,"properties":1902,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1905,"statistic":18},[],{"title":1903},{"VI":1904},"Carol Davila University of Medicine and Pharmacy, Bucharest, Romania",[],{"id":1907,"sortIndex":190,"affiliation":1908,"properties":1914},"8e055361-c0c4-4872-a789-0d0a0a4873b4",{"id":1907,"createTime":18,"updateTime":18,"relativeEntities":1909,"slug":18,"properties":1910,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1913,"statistic":18},[],{"title":1911},{"VI":1912},"Bagdasar-Arseni Clinical Emergency Hospital, Department of Neurosurgery, Bucharest, Romania",[],{},{"title":1916},{"VI":1917},"George E. 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Sabo",{"id":1934,"sortIndex":136,"researcher":18,"roles":1935,"affiliations":1936,"properties":1945,"displayName":1947,"givenName":18,"familyName":18},"55be31f1-5e94-49c7-b364-a30143d65360",[1013],[1937],{"id":1938,"sortIndex":19,"affiliation":1939,"properties":18},"10a60eb0-e0a6-40bd-9761-a4a065a3e707",{"id":1938,"createTime":18,"updateTime":18,"relativeEntities":1940,"slug":18,"properties":1941,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1944,"statistic":18},[],{"title":1942},{"VI":1943},"Elias Clinical Emergency Hospital, Anaesthesiology and Critical Care Department, Bucharest, Romania",[],{"title":1946},{"VI":1947},"Ligia I. Torsin",{"id":1949,"sortIndex":192,"researcher":18,"roles":1950,"affiliations":1951,"properties":1969,"displayName":1971,"givenName":18,"familyName":18},"0d1e7c94-9deb-47d2-9e9a-d99ee4ca55dd",[1013],[1952,1960],{"id":1953,"sortIndex":19,"affiliation":1954,"properties":18},"16ed32ec-0924-47af-b29d-68595fd4da3d",{"id":1953,"createTime":18,"updateTime":18,"relativeEntities":1955,"slug":18,"properties":1956,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1959,"statistic":18},[],{"title":1957},{"VI":1958},"Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, USA",[],{"id":1961,"sortIndex":190,"affiliation":1962,"properties":1968},"d75a858d-dd98-4e73-ac5b-c3499c5671c4",{"id":1961,"createTime":18,"updateTime":18,"relativeEntities":1963,"slug":18,"properties":1964,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1967,"statistic":18},[],{"title":1965},{"VI":1966},"Center for RNA Interference and Non-Coding RNAs, The University of Texas MD Anderson Cancer Center, Houston, USA",[],{},{"title":1970},{"VI":1971},"George A. Calin",{"id":1973,"sortIndex":195,"researcher":18,"roles":1974,"affiliations":1975,"properties":1982,"displayName":1984,"givenName":18,"familyName":18},"8c04b46a-f45a-46fa-9de9-7f26c9ad623e",[1013],[1976],{"id":1953,"sortIndex":19,"affiliation":1977,"properties":18},{"id":1953,"createTime":18,"updateTime":18,"relativeEntities":1978,"slug":18,"properties":1979,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1981,"statistic":18},[],{"title":1980},{"VI":1958},[],{"title":1983},{"VI":1984},"Mihnea P. Dragomir",{"url":1892,"publisher":1986,"properties":2031},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1987,"slug":10,"properties":1988,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1991,"manageAffiliations":2000,"indexDatabases":2011,"url":84,"thumbnailPath":18,"statistic":2026,"gsStatistic":18,"type":155,"analyzePriority":18},[],{"issn":1989,"title":1990},{"VOID":13},{"EN":15},[1992,1996],{"id":22,"createTime":18,"updateTime":18,"relativeEntities":1993,"label":1994,"description":1995,"parentId":18,"standard":18,"scholarHubFieldId":18},[],{"EN":25},{},{"id":28,"createTime":18,"updateTime":18,"relativeEntities":1997,"label":1998,"description":1999,"parentId":18,"standard":18,"scholarHubFieldId":18},[],{"EN":31},{},[2001,2006],{"id":35,"createTime":18,"updateTime":18,"relativeEntities":2002,"slug":18,"properties":2003,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2005,"statistic":18},[],{"title":2004},{"EN":39},[],{"id":42,"createTime":18,"updateTime":18,"relativeEntities":2007,"slug":18,"properties":2008,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2010,"statistic":18},[],{"title":2009},{"EN":46},[],[2012,2019],{"id":50,"indexDatabase":2013,"url":61,"indexYears":62,"academicFieldIds":2018,"indexDatabaseRanking":66},{"id":52,"createTime":18,"updateTime":18,"relativeEntities":2014,"label":2015,"description":2016,"key":58,"publicationTags":2017,"standard":18},[],{"EN":55,"VI":55},{"EN":55,"VI":57},[60],[64,65],{"id":68,"indexDatabase":2020,"url":81,"indexYears":18,"academicFieldIds":2025,"indexDatabaseRanking":18},{"id":70,"createTime":18,"updateTime":18,"relativeEntities":2021,"label":2022,"description":2023,"key":77,"publicationTags":2024,"standard":18},[],{"EN":73,"VI":73},{"EN":75,"VI":76},[79,80],[83],{"impactFactor":19,"impactFactorByYear":2027,"i10Index":99,"i10IndexLast5Year":100,"totalPublication":101,"totalPublicationByYear":2028,"totalCitation":119,"totalCitationByYear":2029,"totalCitationPerPublication":137,"totalCitationPerPublicationByYear":2030,"hindexLast5Year":154,"hindex":154},{"2012":87,"2013":88,"2014":89,"2015":90,"2016":91,"2017":92,"2018":93,"2019":94,"2020":95,"2021":96,"2022":97,"2023":98},{"2008":103,"2009":104,"2010":105,"2011":106,"2012":107,"2013":108,"2014":109,"2015":104,"2016":110,"2017":111,"2018":112,"2019":113,"2020":114,"2021":115,"2022":116,"2023":117,"2024":118},{"2008":121,"2009":122,"2010":123,"2011":124,"2012":125,"2013":126,"2014":127,"2015":128,"2016":129,"2017":130,"2018":131,"2019":132,"2020":133,"2021":134,"2022":135,"2024":136},{"2008":96,"2009":139,"2010":140,"2011":141,"2012":142,"2013":143,"2014":144,"2015":145,"2016":146,"2017":147,"2018":148,"2019":149,"2020":150,"2021":151,"2022":152,"2024":153},{"pages":2032,"volume":2034},{"VOID":2033},"1-21",{"VOID":2035},"38","2019-05-29",2019,[66,79],{"id":2040,"createTime":2041,"updateTime":2042,"relativeEntities":2043,"slug":2044,"properties":2045,"entityType":1006,"verifyStatus":178,"verifyTime":2042,"verifyNote":1007,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":2054,"fullTextUrl":18,"authors":2055,"publicationType":1132,"publisherRelationship":2125,"citationCount":18,"citationInfo":18,"publishDate":2175,"publishYear":2037,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":2176,"openAccess":18,"references":18,"isForceReanalyzing":1187},"010394f9-cdcd-4d7f-8716-b269aad773dd","2023-12-07T10:32:44.919+00:00","2024-12-12T07:21:20.162+00:00",[],"Nek2B-activates-the-wnt-pathway-and-promotes-triple-negative-breast-cancer-chemothezrapy-resistance-by-stabilizing-%CE%B2-catenin",{"abstract":2046,"title":2048,"references":2050,"doi":2052},{"EN":2047},"The chemotherapy-resistance of triple-negative breast cancer (TNBC) remains a major challenge. The Nek2B kinase and β-catenin serve as crucial regulators of mitotic processes. The aim of this study was to test the correlation between Nek2B and TNBC chemotherapy sensitivity, and to determine the regulation of Nek2B on β-catenin and wnt\u002Fβ-catenin signal pathway. Gene Expression Omnibus(GEO) databases were used to gather gene exprsssion data of TNBC patients who undergoing chemotherapy. The co-expression of Nek2B and β-catenin in TNBC surgical sections and cells were analysed by immunohistochemistry, Q-RT-PCR, Western-blot and immunofluorescent staining. The impact of the expression of Nek2B and β-catenin in prognosis was also assessed using the Kaplan-Meier curves. CCK8 assay was used to detect the IC50 value of TNBC cell line. The endogenous binding capacity of Nek2B and β-catenin and phosphorylation of β-catenin by Nek2B were detected using co-immunoprecipitation (CO-IP). Chromatin immune-precipitation (ChIP) analysis and Luciferase Assays were used to evaluate the binding ability of the Nek2B, β-catenin and TCF4 complex with LEF-1 promoter. Nek2B-siRNA and Nek2B plasmid were injected into nude mice, and tumorigenesis was monitored. We found that overexpression of Nek2B and β-catenin in TNBC samples, was associated with patients poor prognosis. Patients with positive Nek2B expression were less sensitive to paclitaxel-containing neoadjuvant chemotherapy. Interestingly, in a panel of established TNBC cell line, Nek2B and β-catenin were highly expressed in cells exhibiting paclitaxel resistance. Our data also suggest that β-catenin binded to and was phosphorylated by Nek2B, and was in a complex with TCF4. Nek2B mainly regulates the expression of β-catenin in TNBC nucleus. Nek2B, β-catenin and TCF4 can be binded with the WRE functional area of LEF-1 promoter. Nek2B can activite wnt signaling pathway and wnt downstream target genes. The tumors treated by Nek2B siRNA associated with paclitaxel were the smallest in nude mouse, and Nek2B can regulate the expression of β-catenin and wnt downstream target genes in vivo. Our study suggested that Nek2B can bind to β-catenin and the co-expression correlated with TNBC patients poor prognosis. It appears that Nek2B and β-catenin might synergize to promote chemotherapy resistance.",{"EN":2049},"Nek2B activates the wnt pathway and promotes triple-negative breast cancer chemothezrapy-resistance by stabilizing β-catenin",{"VOID":2051},"He Y, Jiang Z, Chen C, Wang X. Classification of triple-negative breast cancers based on Immunogenomic profiling. J Exp Clin Cancer Res. 2018;37:327.\nTemian DC, Pop LA, Irimie AI, Berindan-Neagoe I. The epigenetics of triple-negative and basal-like breast Cancer: current knowledge. J Breast Cancer. 2018;21(3):233–43.\nSu Y, Hopfinger NR, Nguyen TD, Pogash TJ, Santucci-Pereira J, Russo J. Epigenetic reprogramming of epithelial mesenchymal transition in triple negative breast cancercells with DNA methyltransferase and histone deacetylase inhibitors. J Exp Clin Cancer Res. 2018;37:314.\nLogue SE, McGrath EP, Cleary P, Greene S, Mnich K, Almanza A, Chevet E, Dwyer RM, Oommen A, Legembre P, Godey F, Madden EC, Leuzzi B, Obacz J, Zeng Q, Patterson JB, Jäger R, Gorman AM, Samali A. Inhibition of IRE1 RNase activity modulates the tumor cell secretome and enhances response to chemotherapy. Nat Commun. 2018;9:3267.\nUto K, Sagata N. Nek2B, a novel maternal form of Nek2 kinase, is essential for the assembly or maintenance of centrosomes in early Xenopus embryos. EMBO J. 2000;19(8):1816–26.\nFang Y, Zhang X. Targeting NEK2 as a promising therapeutic approach for cancer treatment. Cell Cycle. 2016;15(7):895–907.\nZeng Y-R, Han Z-D, Wang C, Cai C, Huang Y-Q, Luo H-W, Liu Z-Z, Zhuo Y-J, Dai Q-S, Zhao H-B, Liang Y-X, Zhong W-D. Overexpression of NIMA-related kinase 2 is associated with progression and poor prognosis of prostate cancer. BMC Urol. 2015;15:90.\nLee J, Gollahon L. Nek2-targeted ASO or siRNA pretreatment enhances anticancer drug sensitivity in triple-negative breast cancer cells. Int J Oncol. 2013;42(3):839–47.\nMarina M, Saavedra HI. Nek2 and Plk4: prognostic markers, drivers of breast tumorigenesis and drug resistance. Front Biosci (Landmark Ed). 2014;19:352–65.\nYang Y, Lei H, Qiang Y-w, Wang B. Ixazomib enhances parathyroid hormone–induced β-catenin\u002FT-cell factor signaling by dissociating β-catenin from the parathyroid hormone receptor. Mol Biol Cell. 2017;28(13):1792–803.\nLin Y-Y, Hsu Y-H, Huang H-Y, Shann Y-J, Huang C-YF, Wei S-C, Chen C-L, Jou T-S. Aberrant nuclear localization of EBP50 promotes colorectal carcinogenesis in xenotransplanted mice by modulating TCF-1 and β-catenin interactions. J Clin Invest. 2012;122(5):1881–94.\nSu H, Sureda-Gomez M, Rabaneda-Lombarte N, Gelabert M, Xie J, Wu W, Adell T. A C-terminally truncated form of β-catenin acts as a novel regulator of Wnt\u002Fβ-catenin signaling in planarians. PLoS Genet. 2017;13(10):e1007030.\nBahmanyar S, Kaplan DD, DeLuca JG, Giddings TH Jr, O’Toole ET, Winey M, Salmon ED, Casey PJ, Nelson WJ, Barth AIM. β-Catenin is a Nek2 substrate involved in centrosome separation. Genes Dev. 2008;22(1):91–105.\nMbom BC, Siemers KA, Ostrowski MA, Nelson WJ, Barth AIM. Nek2 phosphorylates and stabilizes β-catenin at mitotic centrosomes downstream of Plk1. Mol Biol Cell. 2014;25(7):977–91.\nShen H, Yang Y, Zhao L, Yuan J, Niu Y. Lin28A and androgen receptor expression in ER−\u002FHer2+ breast cancer. Breast Cancer Res Treat. 2016;156(1):135–47.\nWang Y, Shen H, Yin Q, Zhang T, Liu Z, Zhang W, Niu Y. Effect of NIMA-related kinase 2B on the sensitivity of breast cancer to paclitaxel in vitro and vivo. Tumour Biol. 2017;39(5):1010428317699754.\nWang J, Cheng P, Pavlyukov MS, Yu H, Zhang Z, Kim S-H, Minata M, Mohyeldin A, Xie W, Chen D, Goidts V, Frett B, Hu W, Li H, Shin YJ, Lee Y, Nam D-H, Kornblum HI, Wang M, Nakano I. Targeting NEK2 attenuates glioblastoma growth and radioresistance by destabilizing histone methyltransferase EZH2. J Clin Invest. 2017;127(8):3075–89.\nFranqui-Machin R, Hao M, Bai H, Gu Z, Zhan X, Habelhah H, Jethava Y, Qiu L, Frech I, Tricot G, Zhan F. Destabilizing NEK2 overcomes resistance to proteasome inhibition in multiple myeloma. J Clin Invest. 2018;128(7):2877–93.\nKim S, Lee K, Choi J-H, Ringstad N, Dynlacht BD. Nek2 activation of Kif24 ensures cilium disassembly during the cell cycle. Nat Commun. 2015;6:8087.\nSinha A, Agarwal S, Parashar D, Verma A, Saini S, Jagadish N, Ansari AS, Lohiya NK, Suri A. Down regulation of SPAG9 reduces growth and invasive potential of triple-negative breast cancercells: possible implications in targeted therapy. 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J Surg Oncol. 2014;110:828–38.\nLee J, Gollahon L. Mitotic perturbations induced by Nek2 overexpression require interaction with TRF1 in breast cancer cells. Cell Cycle. 2013;12(23):3599–614.",{"VOID":2053},"10.1186\u002Fs13046-019-1231-y","https:\u002F\u002Fjeccr.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13046-019-1231-y",[2056,2071,2084,2099,2112],{"id":2057,"sortIndex":19,"researcher":18,"roles":2058,"affiliations":2059,"properties":2068,"displayName":2070,"givenName":18,"familyName":18},"1b8c38ff-c98d-42d5-b8f3-edf91b5b7426",[1013],[2060],{"id":2061,"sortIndex":19,"affiliation":2062,"properties":18},"3e1d3822-be8f-4d45-b105-88479130c348",{"id":2061,"createTime":18,"updateTime":18,"relativeEntities":2063,"slug":18,"properties":2064,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2067,"statistic":18},[],{"title":2065},{"VI":2066},"Department of pathology, The Second Clinical Medical College, Shanxi Medical University, Taiyuan, People’s Republic of China",[],{"title":2069},{"VI":2070},"Honghong Shen",{"id":2072,"sortIndex":190,"researcher":18,"roles":2073,"affiliations":2074,"properties":2081,"displayName":2083,"givenName":18,"familyName":18},"19611140-7585-42f2-a4a4-471b6d9f7500",[1013],[2075],{"id":2061,"sortIndex":19,"affiliation":2076,"properties":18},{"id":2061,"createTime":18,"updateTime":18,"relativeEntities":2077,"slug":18,"properties":2078,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2080,"statistic":18},[],{"title":2079},{"VI":2066},[],{"title":2082},{"VI":2083},"Wenpeng Yan",{"id":2085,"sortIndex":136,"researcher":18,"roles":2086,"affiliations":2087,"properties":2096,"displayName":2098,"givenName":18,"familyName":18},"b250fe38-295d-435c-8deb-b124e5ae4df9",[1013],[2088],{"id":2089,"sortIndex":19,"affiliation":2090,"properties":18},"24b6c535-f67b-4cae-beee-be165dbbcd75",{"id":2089,"createTime":18,"updateTime":18,"relativeEntities":2091,"slug":18,"properties":2092,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2095,"statistic":18},[],{"title":2093},{"VI":2094},"Department of general surgery, The Second Clinical Medical College, Shanxi Medical University, Taiyuan, People’s Republic of China",[],{"title":2097},{"VI":2098},"Jinyang Yuan",{"id":2100,"sortIndex":192,"researcher":18,"roles":2101,"affiliations":2102,"properties":2109,"displayName":2111,"givenName":18,"familyName":18},"225eeb37-6d67-4bc7-a42a-bafbe99eb511",[1013],[2103],{"id":2061,"sortIndex":19,"affiliation":2104,"properties":18},{"id":2061,"createTime":18,"updateTime":18,"relativeEntities":2105,"slug":18,"properties":2106,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2108,"statistic":18},[],{"title":2107},{"VI":2066},[],{"title":2110},{"VI":2111},"Ziyue Wang",{"id":2113,"sortIndex":195,"researcher":18,"roles":2114,"affiliations":2115,"properties":2122,"displayName":2124,"givenName":18,"familyName":18},"6c078dd1-eb10-4b7c-9d11-5f0d8ec00a65",[1013],[2116],{"id":2061,"sortIndex":19,"affiliation":2117,"properties":18},{"id":2061,"createTime":18,"updateTime":18,"relativeEntities":2118,"slug":18,"properties":2119,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2121,"statistic":18},[],{"title":2120},{"VI":2066},[],{"title":2123},{"VI":2124},"Chen Wang",{"url":2054,"publisher":2126,"properties":2171},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":2127,"slug":10,"properties":2128,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":2131,"manageAffiliations":2140,"indexDatabases":2151,"url":84,"thumbnailPath":18,"statistic":2166,"gsStatistic":18,"type":155,"analyzePriority":18},[],{"issn":2129,"title":2130},{"VOID":13},{"EN":15},[2132,2136],{"id":22,"createTime":18,"updateTime":18,"relativeEntities":2133,"label":2134,"description":2135,"parentId":18,"standard":18,"scholarHubFieldId":18},[],{"EN":25},{},{"id":28,"createTime":18,"updateTime":18,"relativeEntities":2137,"label":2138,"description":2139,"parentId":18,"standard":18,"scholarHubFieldId":18},[],{"EN":31},{},[2141,2146],{"id":35,"createTime":18,"updateTime":18,"relativeEntities":2142,"slug":18,"properties":2143,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2145,"statistic":18},[],{"title":2144},{"EN":39},[],{"id":42,"createTime":18,"updateTime":18,"relativeEntities":2147,"slug":18,"properties":2148,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2150,"statistic":18},[],{"title":2149},{"EN":46},[],[2152,2159],{"id":50,"indexDatabase":2153,"url":61,"indexYears":62,"academicFieldIds":2158,"indexDatabaseRanking":66},{"id":52,"createTime":18,"updateTime":18,"relativeEntities":2154,"label":2155,"description":2156,"key":58,"publicationTags":2157,"standard":18},[],{"EN":55,"VI":55},{"EN":55,"VI":57},[60],[64,65],{"id":68,"indexDatabase":2160,"url":81,"indexYears":18,"academicFieldIds":2165,"indexDatabaseRanking":18},{"id":70,"createTime":18,"updateTime":18,"relativeEntities":2161,"label":2162,"description":2163,"key":77,"publicationTags":2164,"standard":18},[],{"EN":73,"VI":73},{"EN":75,"VI":76},[79,80],[83],{"impactFactor":19,"impactFactorByYear":2167,"i10Index":99,"i10IndexLast5Year":100,"totalPublication":101,"totalPublicationByYear":2168,"totalCitation":119,"totalCitationByYear":2169,"totalCitationPerPublication":137,"totalCitationPerPublicationByYear":2170,"hindexLast5Year":154,"hindex":154},{"2012":87,"2013":88,"2014":89,"2015":90,"2016":91,"2017":92,"2018":93,"2019":94,"2020":95,"2021":96,"2022":97,"2023":98},{"2008":103,"2009":104,"2010":105,"2011":106,"2012":107,"2013":108,"2014":109,"2015":104,"2016":110,"2017":111,"2018":112,"2019":113,"2020":114,"2021":115,"2022":116,"2023":117,"2024":118},{"2008":121,"2009":122,"2010":123,"2011":124,"2012":125,"2013":126,"2014":127,"2015":128,"2016":129,"2017":130,"2018":131,"2019":132,"2020":133,"2021":134,"2022":135,"2024":136},{"2008":96,"2009":139,"2010":140,"2011":141,"2012":142,"2013":143,"2014":144,"2015":145,"2016":146,"2017":147,"2018":148,"2019":149,"2020":150,"2021":151,"2022":152,"2024":153},{"pages":2172,"volume":2174},{"VOID":2173},"1-17",{"VOID":2035},"2019-06-07",[66,79],{"id":2178,"createTime":2179,"updateTime":2180,"relativeEntities":2181,"slug":2182,"properties":2183,"entityType":1006,"verifyStatus":178,"verifyTime":2180,"verifyNote":1007,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":2192,"fullTextUrl":18,"authors":2193,"publicationType":1132,"publisherRelationship":2315,"citationCount":18,"citationInfo":18,"publishDate":2366,"publishYear":2367,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":2368,"openAccess":18,"references":18,"isForceReanalyzing":1187},"010a596c-8ad6-4705-b4d2-08cd689e047b","2024-01-13T21:58:55.248+00:00","2025-02-26T08:05:35.147+00:00",[],"The-oncogenic-kinase-NEK2-regulates-an-RBFOX2-dependent-pro-mesenchymal-splicing-program-in-triple-negative-breast-cancer-cells",{"abstract":2184,"title":2186,"references":2188,"doi":2190},{"EN":2185},"Triple-negative breast cancer (TNBC) is the most heterogeneous and malignant subtype of breast cancer (BC). TNBC is defined by the absence of expression of estrogen, progesterone and HER2 receptors and lacks efficacious targeted therapies. NEK2 is an oncogenic kinase that is significantly upregulated in TNBC, thereby representing a promising therapeutic target. NEK2 localizes in the nucleus and promotes oncogenic splice variants in different cancer cells. Notably, alternative splicing (AS) dysregulation has recently emerged as a featuring trait of TNBC that contributes to its aggressive phenotype. To investigate whether NEK2 modulates TNBC transcriptome we performed RNA-sequencing analyses in a representative TNBC cell line (MDA-MB-231) and results were validated in multiple TNBC cell lines. Bioinformatics and functional analyses were carried out to elucidate the mechanism of splicing regulation by NEK2. Data from The Cancer Genome Atlas were mined to evaluate the potential of NEK2-sensitive exons as markers to identify the TNBC subtype and to assess their prognostic value. Transcriptome analysis revealed a widespread impact of NEK2 on the transcriptome of TNBC cells, with 1830 AS events that are susceptible to its expression. NEK2 regulates the inclusion of cassette exons in splice variants that discriminate TNBC from other BC and that correlate with poor prognosis, suggesting that this kinase contributes to the TNBC-specific splicing program. NEK2 elicits its effects by modulating the expression of the splicing factor RBFOX2, a well-known regulator of epithelial to mesenchymal transition (EMT). Accordingly, NEK2 splicing-regulated genes are enriched in functional terms related to cell adhesion and contractile cytoskeleton and NEK2 depletion in mesenchymal TNBC cells induces phenotypic and molecular traits typical of epithelial cells. Remarkably, depletion of select NEK2-sensitive splice-variants that are prognostic in TNBC patients is sufficient to interfere with TNBC cell morphology and motility, suggesting that NEK2 orchestrates a pro-mesenchymal splicing program that modulates migratory and invasive properties of TNBC cells. Our study uncovers an extensive splicing program modulated by NEK2 involving splice variants that confer an invasive phenotype to TNBCs and that might represent, together with NEK2 itself, valuable therapeutic targets for this disease.",{"EN":2187},"The oncogenic kinase NEK2 regulates an RBFOX2-dependent pro-mesenchymal splicing program in triple-negative breast cancer cells",{"VOID":2189},"Harbeck N, Gnant M. Breast cancer. Lancet. 2017;389:1134–50.\nYeo SK, Guan J. Breast Cancer: multiple subtypes within a tumor? Breast cancer stratification and its role in guiding therapeutic decisions. Trends Cancer. 2018;3:753–60.\nGarrido-Castro AC, Lin NU, Polyak K. 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Cadherin 11 inhibition downregulates β-catenin, deactivates the canonical WNT signalling pathway and suppresses the cancer stem cell-like phenotype of triple negative breast cancer. J Clin Med. 2019;8:148.\nKarihtala P, Auvinen P, Kauppila S, Haapasaari KM, Jukkola-Vuorinen A, Soini Y. Vimentin, zeb1 and Sip1 are up-regulated in triple-negative and basal-like breast cancers: association with an aggressive tumour phenotype. Breast Cancer Res Treat. 2013;138:81–90.\nNaso FD, Boi D, Ascanelli C, Pamfil G, Lindon C, Paiardini A, et al. Nuclear localisation of Aurora-a: its regulation and significance for Aurora-a functions in cancer. Oncogene. 2021;40:3917–28.\nBegg BE, Jens M, Wang PY, Minor CM, Burge CB. Concentration-dependent splicing is enabled by Rbfox motifs of intermediate affinity. Nat Struct Mol Biol. 2020;27:901–12.\nZhou D, Couture S, Scott MS, Abou ES. RBFOX2 alters splicing outcome in distinct binding modes with multiple protein partners. Nucleic Acids Res. 2021;8000:1–14.\nDamianov A, Ying Y, Lin C-H, Lee J-A, Tran D, Vashisht AA, et al. Rbfox proteins regulate splicing as part of a large multiprotein complex LASR. Cell. 2016;165:606–19. Elsevier Inc.\nVenables JP, Brosseau J-P, Gadea G, Klinck R, Prinos P, Beaulieu J-F, et al. RBFOX2 is an important regulator of Mesenchymal tissue-specific splicing in both Normal and Cancer tissues. Mol Cell Biol. 2013;33:396–405.\nLapuk A, Marr H, Jakkula L, Pedro H, Bhattacharya S, Purdom E, et al. Exon-level microarray analyses identify alternative splicing programs in breast Cancer. Mol Cancer Res. 2010;8:961–74.\nDolfini D, Andrioletti V, Mantovani R. Overexpression and alternative splicing of NF-YA in breast cancer. Sci Rep. 2019;9:12955.\nLieberman J. Tapping the RNA world for therapeutics. Nat Struct Mol Biol. 2018;25:357–64.",{"VOID":2191},"10.1186\u002Fs13046-021-02210-3","https:\u002F\u002Fjeccr.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13046-021-02210-3",[2194,2218,2238,2258,2278,2293],{"id":2195,"sortIndex":19,"researcher":18,"roles":2196,"affiliations":2197,"properties":2215,"displayName":2217,"givenName":18,"familyName":18},"d908048d-b8a3-4ffd-9e75-470d3f7ae826",[1013],[2198,2206],{"id":2199,"sortIndex":19,"affiliation":2200,"properties":18},"73d62301-589d-4152-ab5d-644c1bd4eef1",{"id":2199,"createTime":18,"updateTime":18,"relativeEntities":2201,"slug":18,"properties":2202,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2205,"statistic":18},[],{"title":2203},{"VI":2204},"Department of Neuroscience, Section of Human Anatomy, Catholic University of the Sacred Heart, Rome, Italy",[],{"id":2207,"sortIndex":190,"affiliation":2208,"properties":2214},"7cb0a075-4574-4f01-a834-d3055288a600",{"id":2207,"createTime":18,"updateTime":18,"relativeEntities":2209,"slug":18,"properties":2210,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2213,"statistic":18},[],{"title":2211},{"VI":2212},"Fondazione Policlinico Universitario A. 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RNA-binding protein Musashi-2 (MSI2) has been implicated in the tumorigenesis and tumor progression of some human cancers. MSI2 has also been reported to suppress tumor epithelial-to-mesenchymal transition (EMT) progression in breast cancer, and low MSI2 expression is associated with poor outcomes for breast cancer patients; however, the underlying mechanisms have not been fully investigated. This study investigated the expression and phenotypic functions of two major alternatively spliced MSI2 isoforms (MSI2a and MSI2b) and the potential molecular mechanisms involved in triple-negative breast cancer (TNBC) progression. The Illumina sequencing platform was used to analyze the mRNA transcriptomes of TNBC and normal tissues, while quantitative reverse transcription-polymerase chain reaction and immunohistochemistry validated MSI2 isoform expression in breast cancer tissues. The effects of MSI2a and MSI2b on TNBC cells were assayed in vitro and in vivo. RNA immunoprecipitation (RIP) and RNA sequencing were performed to identify the potential mRNA targets of MSI2a, and RIP and luciferase analyses were used to confirm the mRNA targets of MSI2. MSI2 expression in TNBC tissues was significantly downregulated compared to that in normal tissues. In TNBC, MSI2a expression was associated with poor overall survival of patients. MSI2a overexpression in vitro and in vivo inhibited TNBC cell invasion as well as extracellular signal-regulated kinase 1\u002F2 (ERK1\u002F2) activity. However, MSI2b overexpression had no significant effects on TNBC cell migration. Mechanistically, MSI2a expression promoted TP53INP1 mRNA stability by its interaction with the 3′-untranslated region of TP53INP1 mRNA. Furthermore, TP53INP1 knockdown reversed MSI2a-induced suppression of TNBC cell invasion, whereas ectopic expression of TP53INP1 and inhibition of ERK1\u002F2 activity blocked MSI2 knockdown-induced TNBC cell invasion. The current study demonstrated that MSI2a is the predominant functional isoform of MSI2 proteins in TNBC, that its downregulation is associated with TNBC progression and poor prognosis and that MSI2a expression inhibited TNBC invasion by stabilizing TP53INP1 mRNA and inhibiting ERK1\u002F2 activity. Overall, our study provides new insights into the isoform-specific roles of MSI2a and MSI2b in the tumor progression of TNBC, allowing for novel therapeutic strategies to be developed for TNBC.",{"EN":2379},"RNA-binding protein MSI2 isoforms expression and regulation in progression of triple-negative breast cancer",{"VOID":2381},"McGuire A, Brown JA, Malone C, McLaughlin R, Kerin MJ. Effects of age on the detection and management of breast cancer. Cancers (Basel). 2015;7:908–29.\nReeder JG, Vogel VG. Breast cancer prevention. Cancer Treat Res. 2008;141:149–64.\nBose S. Triple-negative breast carcinoma: morphologic and molecular subtypes. Adv Anat Pathol. 2015;22:306–13.\nSharma P. Biology and Management of Patients with triple-negative breast Cancer. Oncologist. 2016;21:1050–62.\nDent R, Trudeau M, Pritchard KI, Hanna WM, Kahn HK, Sawka CA, et al. Triple-negative breast Cancer: clinical features and patterns of recurrence. Clin Cancer Res. 2007;13:4429–34.\nBerrada N, Delaloge S, André F. Treatment of triple-negative metastatic breast cancer: toward individualized targeted treatments or chemosensitization? Ann Oncol. 2010;21:i30–5.\nPereira B, Billaud M, Almeida R. RNA-binding proteins in Cancer: old players and new actors. Trends Cancer. 2017;3:506–28.\nHong S. RNA binding protein as an emerging therapeutic target for Cancer prevention and treatment. J Cancer Prev. 2017;22:203–10.\nKudinov AE, Karanicolas J, Golemis EA, Boumber Y. Musashi RNA-binding proteins as Cancer drivers and novel therapeutic targets. Clin Cancer Res. 2017;23:2143–53.\nKharas MG, Lengner CJ. Stem cells, Cancer, and MUSASHI in blood and guts. Trends Cancer. 2017;3:347–56.\nByers RJ, Currie T, Tholouli E, Rodig SJ, Kutok JL. MSI2 protein expression predicts unfavorable outcome in acute myeloid leukemia. Blood. 2011;118:2857–67.\nKudinov AE, Deneka A, Nikonova AS, Beck TN, Ahn Y, Liu X, et al. Musashi-2 (MSI2) supports TGF-β signaling and inhibits claudins to promote non-small cell lung cancer (NSCLC) metastasis. Proc Natl Acad Sci. 2016;113:6955–60.\nSzabat M, Kalynyak TB, Lim GE, Chu KY, Yang YH, Asadi A, et al. Musashi expression in beta-cells coordinates insulin expression, apoptosis and proliferation in response to endoplasmic reticulum stress in diabetes. Cell Death Dis. 2011;2:e232.\nKatz Y, Li F, Lambert NJ, Sokol ES, Tam WL, Cheng AW, et al. Musashi proteins are post-transcriptional regulators of the epithelial-luminal cell state. Elife. 2014;3:e3915.\nKang MH, Jeong KJ, Kim WY, Lee HJ, Gong G, Suh N, et al. Musashi RNA-binding protein 2 regulates estrogen receptor 1 function in breast cancer. Oncogene. 2017;36:1745–52.\nWuebben EL, Mallanna SK, Cox JL, Rizzino A. Musashi2 is required for the self-renewal and pluripotency of embryonic stem cells. PLoS One. 2012;7:e34827.\nMacNicol MC, Cragle CE, McDaniel FK, Hardy LL, Wang Y, Arumugam K, et al. Evasion of regulatory phosphorylation by an alternatively spliced isoform of Musashi2. Sci Rep. 2017;7:11503.\nLi M, Li A, Zhou S, Lv H, Yang W. SPAG5 upregulation contributes to enhanced c-MYC transcriptional activity via interaction with c-MYC binding protein in triple-negative breast cancer. J Hematol Oncol. 2019;12:14.\nNg K, Chan L, Chai S, Tong M, Guan X, Lee NP, et al. TP53INP1 Downregulation activates a p73-dependent DUSP10\u002FERK signaling pathway to promote metastasis of hepatocellular carcinoma. Cancer Res. 2017;77:4602–12.\nSamanta S, Sharma VM, Khan A, Mercurio AM. Regulation of IMP3 by EGFR signaling and repression by ERβ: implications for triple-negative breast cancer. Oncogene. 2012;31:4689–97.\nSamanta S, Sun H, Goel HL, Pursell B, Chang C, Khan A, et al. IMP3 promotes stem-like properties in triple-negative breast cancer by regulating SLUG.Oncogene. 2016;35:1111–21.\nMiles WO, Lembo A, Volorio A, Brachtel E, Tian B, Sgroi D, et al. Alternative Polyadenylation in triple-negative breast tumors allows NRAS and c-JUN to bypass PUMILIO posttranscriptional regulation. Cancer Res. 2016;76:7231–41.\nKharas MG, Lengner CJ, Al-Shahrour F, Bullinger L, Ball B, Zaidi S, et al. Musashi-2 regulates normal hematopoiesis and promotes aggressive myeloid leukemia. Nat Med. 2010;16:903–8.\nPark SM, Deering RP, Lu Y, Tivnan P, Lianoglou S, Al-Shahrour F, et al. Musashi-2 controls cell fate, lineage bias, and TGF-beta signaling in HSCs. J Exp Med. 2014;211:71–87.\nWang S, Li N, Yousefi M, Nakauka-Ddamba A, Li F, Parada K, et al. Transformation of the intestinal epithelium by the MSI2 RNA-binding protein. Nat Commun. 2015;6:6517.\nBennett CG, Riemondy K, Chapnick DA, Bunker E, Liu X, Kuersten S, et al. Genome-wide analysis of Musashi-2 targets reveals novel functions in governing epithelial cell migration. Nucleic Acids Res. 2016;44:3788–800.\nChoi YM, Kim KB, Lee JH, Chun YK, An IS, An S, et al. DBC2\u002FRhoBTB2 functions as a tumor suppressor protein via Musashi-2 ubiquitination in breast cancer. Oncogene. 2017;36:2802–12.\nChien MH, Lee WJ, Yang YC, Li YL, Chen BR, Cheng TY, et al. KSRP suppresses cell invasion and metastasis through miR-23a-mediated EGR3 mRNA degradation in non-small cell lung cancer. Biochim Biophys Acta Gene Regul Mech. 1860;2017:1013–24.\nPruksakorn D, Teeyakasem P, Klangjorhor J, Chaiyawat P, Settakorn J, Diskul-Na-Ayudthaya P, et al. Overexpression of KH-type splicing regulatory protein regulates proliferation, migration, and implantation ability of osteosarcoma. Int J Oncol. 2016;49:903–12.\nShahbazi J, Lock R, Liu T. Tumor protein 53-induced nuclear protein 1 enhances p53 function and represses tumorigenesis. Front Genet. 2013;4:80.\nAnn EJ, Kim MY, Yoon JH, Ahn JS, Jo EH, Lee HJ, et al. Tumor suppressor HIPK2 regulates malignant growth via phosphorylation of Notch1. Cancer Res. 2016;76:4728–40.\nAbdel-Fatah T, Arora A, Agarwal D, Moseley P, Perry C, Thompson N, et al. Adverse prognostic and predictive significance of low DNA-dependent protein kinase catalytic subunit (DNA-PKcs) expression in early-stage breast cancers. Breast Cancer Res Tr. 2014;146:309–20.\nHallajian Z, Mahjoubi F, Nafissi N. Simultaneous ATM\u002FBRCA1\u002FRAD51 expression variations associated with prognostic factors in Iranian sporadic breast cancer patients. Breast Cancer-Tokyo. 2017;24:624–34.\nAsaduzzaman M, Constantinou S, Min H, Gallon J, Lin M, Singh P, et al. Tumour suppressor EP300, a modulator of paclitaxel resistance and stemness, is downregulated in metaplastic breast cancer. Breast Cancer Res Tr. 2017;163:461–74.\nKrishnamurthy S, Poornima R, Challa VR, Goud YG. Triple negative breast cancer - our experience and review. Indian J Surg Oncol. 2012;3:12–6.\nOkamura S, Arakawa H, Tanaka T, Nakanishi H, Ng CC, Taya Y, et al. p53DINP1, a p53-inducible gene, regulates p53-dependent. Apoptosis. 2001;8:85–94.\nTomasini R, Seux M, Nowak J, Bontemps C, Carrier A, Dagorn JC, et al. TP53INP1 is a novel p73 target gene that induces cell cycle arrest and cell death by modulating p73 transcriptional activity. Oncogene. 2005;24:8093–104.\nSeux M, Peuget S, Montero MP, Siret C, Rigot V, Clerc P, et al. TP53INP1 decreases pancreatic cancer cell migration by regulating SPARC expression. Oncogene. 2011;30:3049–61.\nSankpal NV, Fleming TP, Sharma PK, Wiedner HJ, Gillanders WE. A double-negative feedback loop between EpCAM and ERK contributes to the regulation of epithelial–mesenchymal transition in cancer. Oncogene. 2017;36:3706–17.\nLow HB, Zhang Y. Regulatory roles of MAPK phosphatases in Cancer. Immune Netw. 2016;16:85.\nPachmayr E, Treese C, Stein U. Underlying mechanisms for distant metastasis - molecular biology. Visc Med. 2017;33:11–20.",{"VOID":2383},"10.1186\u002Fs13046-020-01587-x","https:\u002F\u002Fjeccr.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs13046-020-01587-x",[2386,2419,2446,2473,2500,2536],{"id":2387,"sortIndex":19,"researcher":18,"roles":2388,"affiliations":2389,"properties":2416,"displayName":2418,"givenName":18,"familyName":18},"3b20b5d2-5caf-471a-bc8e-1c5c0fb64196",[1013],[2390,2398,2407],{"id":2391,"sortIndex":19,"affiliation":2392,"properties":18},"19115f35-7f1c-4417-8092-e0403e049400",{"id":2391,"createTime":18,"updateTime":18,"relativeEntities":2393,"slug":18,"properties":2394,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2397,"statistic":18},[],{"title":2395},{"VI":2396},"Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 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dynamics homeostasis is important for cell metabolism, growth, proliferation, and immune responses. The critical GTPase for mitochondrial fission, Drp1 is frequently upregulated in many cancers and is closely implicated in tumorigenesis. However, the mechanism underling Drp1 to influence tumor progression is largely unknown, especially in esophageal squamous cell carcinoma (ESCC). Immunohistochemistry was used to examine Drp1 and LC3B expression in tissues of ESCC patients. Autophagic vesicles were investigated by transmission electron microscopy. Fluorescent LC3B puncta and mitochondrial nucleoid were observed by fluorescent and confocal microscopy. Mitochondrial function was evaluated by mitochondrial membrane potential, ROS and ATP levels. Xenograft tumor model was performed in BALB\u002Fc nude mice to analyze the role of Drp1 on ESCC progression. We found that Drp1 high expression is correlated with poor overall survival of ESCC patients. Drp1 overexpression promotes cell proliferation and xenograft ESCC tumor growth by triggering autophagy. Furthermore, we demonstrated that Drp1 overexpression disturbs mitochondrial function and subsequent induces mitochondrial DNA (mtDNA) released into the cytosol thereby inducing cytosolic mtDNA stress. Mechanistically, cytosolic mtDNA activates the cGAS-STING pathway and facilitates autophagy, which promotes ESCC cancer growth. Moreover, mtDNA digestion with DNase I and autophagy inhibition with chloroquine attenuates the cGAS-STING pathway activation and ESCC cancer growth. Our finding reveals that Drp1 overexpression induces mitochondrial dysfunction and cytosolic mtDNA stress, which subsequently activates the cGAS-STING pathway, triggers autophagy and promotes ESCC progression.",{"EN":2627},"Increased Drp1 promotes autophagy and ESCC progression by mtDNA stress mediated cGAS-STING pathway",{"VOID":2629},"West AP, Shadel GS, Ghosh S. Mitochondria in innate immune responses. Nat Rev Immunol. 2011;11(6):389–402.\nWest AP, Khoury-Hanold W, Staron M, Tal MC, Pineda CM, Lang SM, et al. Mitochondrial DNA stress primes the antiviral innate immune response. Nature. 2015;520(7548):553–7.\nVyas S, Zaganjor E, Haigis MC. Mitochondria and Cancer. Cell. 2016;166(3):555–66.\nWallace DC. Mitochondria and cancer. Nat Rev Cancer. 2012;12(10):685–98.\nRehman J, Zhang HJ, Toth PT, Zhang Y, Marsboom G, Hong Z, et al. Inhibition of mitochondrial fission prevents cell cycle progression in lung cancer. FASEB J. 2012;26(5):2175–86.\nHuang Q, Zhan L, Cao H, Li J, Lyu Y, Guo X, et al. Increased mitochondrial fission promotes autophagy and hepatocellular carcinoma cell survival through the ROS-modulated coordinated regulation of the NFKB and TP53 pathways. Autophagy. 2016;12(6):999–1014.\nGrazioli S, Pugin J. Mitochondrial Damage-Associated Molecular Patterns: From Inflammatory Signaling to Human Diseases. Front Immunol. 2018;9:832.\nKrysko DV, Agostinis P, Krysko O, Garg AD, Bachert C, Lambrecht BN, et al. Emerging role of damage-associated molecular patterns derived from mitochondria in inflammation. Trends Immunol. 2011;32(4):157–64.\nLiu S, Feng M, Guan W. Mitochondrial DNA sensing by STING signaling participates in inflammation, cancer and beyond. Int J Cancer. 2016;139(4):736–41.\nWest AP, Shadel GS. Mitochondrial DNA in innate immune responses and inflammatory pathology. Nat Rev Immunol. 2017;17(6):363–75.\nLiu Y, Yan W, Tohme S, Chen M, Fu Y, Tian D, et al. Hypoxia induced HMGB1 and mitochondrial DNA interactions mediate tumor growth in hepatocellular carcinoma through Toll-like receptor 9. J Hepatol. 2015;63(1):114–21.\nBao D, Zhao J, Zhou X, Yang Q, Chen Y, Zhu J, et al. Mitochondrial fission-induced mtDNA stress promotes tumor-associated macrophage infiltration and HCC progression. Oncogene. 2019;38(25):5007–20.\nAblasser A, Goldeck M, Cavlar T, Deimling T, Witte G, Röhl I, et al. cGAS produces a 2′-5′-linked cyclic dinucleotide second messenger that activates STING. Nature. 2013;498(7454):380–4.\nGao P, Ascano M, Wu Y, Barchet W, Gaffney BL, Zillinger T, et al. Cyclic [G(2’,5’)pA(3’,5’)p] is the metazoan second messenger produced by DNA-activated cyclic GMP-AMP synthase. Cell. 2013;153(5):1094–107.\nBarber GN. STING: infection, inflammation and cancer. Nat Rev Immunol. 2015;15(12):760–70.\nKhoo LT, Chen LY. Role of the cGAS-STING pathway in cancer development and oncotherapeutic approaches. EMBO Rep. 2018;19(12).\nSu T, Zhang Y, Valerie K, Wang XY, Lin S, Zhu G. STING activation in cancer immunotherapy. Theranostics. 2019;9(25):7759–71.\nWang Y, Luo J, Alu A, Han X, Wei Y, Wei X. cGAS-STING pathway in cancer biotherapy. Mol Cancer. 2020;19(1):136.\nWoo SR, Fuertes MB, Corrales L, Spranger S, Furdyna MJ, Leung MY, et al. STING-dependent cytosolic DNA sensing mediates innate immune recognition of immunogenic tumors. Immunity. 2014;41(5):830–42.\nSnell LM, McGaha TL, Brooks DG. Type I Interferon in Chronic Virus Infection and Cancer. Trends Immunol. 2017;38(8):542–57.\nChen Q, Boire A, Jin X, Valiente M, Er EE, Lopez-Soto A, et al. Carcinoma-astrocyte gap junctions promote brain metastasis by cGAMP transfer. Nature. 2016;533(7604):493–8.\nKwon J, Bakhoum SF. The Cytosolic DNA-Sensing cGAS-STING Pathway in Cancer. Cancer Discov. 2020;10(1):26–39.\nLemos H, Mohamed E, Huang L, Ou R, Pacholczyk G, Arbab AS, et al. STING Promotes the Growth of Tumors Characterized by Low Antigenicity via IDO Activation. Cancer Res. 2016;76(8):2076–81.\nNg KW, Marshall EA, Bell JC, Lam WL. cGAS-STING and Cancer: Dichotomous Roles in Tumor Immunity and Development. Trends Immunol. 2018;39(1):44–54.\nZheng J, Mo J, Zhu T, Zhuo W, Yi Y, Hu S, et al. Comprehensive elaboration of the cGAS-STING signaling axis in cancer development and immunotherapy. Mol Cancer. 2020;19(1):133.\nWhite MJ, McArthur K, Metcalf D, Lane RM, Cambier JC, Herold MJ, et al. Apoptotic caspases suppress mtDNA-induced STING-mediated type I IFN production. Cell. 2014;159(7):1549–62.\nRongvaux A, Jackson R, Harman CC, Li T, West AP, de Zoete MR, et al. Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA. Cell. 2014;159(7):1563–77.\nMizushima N, Levine B, Cuervo AM, Klionsky DJ. Autophagy fights disease through cellular self-digestion. Nature. 2008;451(7182):1069–75.\nKroemer G, Marino G, Levine B. Autophagy and the integrated stress response. Mol Cell. 2010;40(2):280–93.\nAmaravadi RK, Lippincott-Schwartz J, Yin XM, Weiss WA, Takebe N, Timmer W, et al. Principles and current strategies for targeting autophagy for cancer treatment. Clin Cancer Res. 2011;17(4):654–66.\nKatheder NS, Khezri R, O’Farrell F, Schultz SW, Jain A, Rahman MM, et al. Microenvironmental autophagy promotes tumour growth. Nature. 2017;541(7637):417–20.\nMaes H, Rubio N, Garg AD, Agostinis P. Autophagy: shaping the tumor microenvironment and therapeutic response. Trends Mol Med. 2013;19(7):428–46.\nGao W, Guo H, Niu M, Zheng X, Zhang Y, Xue X, et al. circPARD3 drives malignant progression and chemoresistance of laryngeal squamous cell carcinoma by inhibiting autophagy through the PRKCI-Akt-mTOR pathway. Mol Cancer. 2020;19(1):166.\nBoland ML, Chourasia AH, Macleod KF. Mitochondrial dysfunction in cancer. Front. Oncol. 2013;3:292.\nGui X, Yang H, Li T, Tan X, Shi P, Li M, et al. Autophagy induction via STING trafficking is a primordial function of the cGAS pathway. Nature. 2019;567(7747):262–6.\nPrabakaran T, Bodda C, Krapp C, Zhang BC, Christensen MH, Sun C, et al. Attenuation of cGAS-STING signaling is mediated by a p62\u002FSQSTM1-dependent autophagy pathway activated by TBK1. EMBO J. 2018;37(8):e97858.\nKim J, Gupta R, Blanco LP, Yang S, Shteinfer-Kuzmine A, Wang K, et al. VDAC oligomers form mitochondrial pores to release mtDNA fragments and promote lupus-like disease. Science. 2019;366(6472):1531–6.\nMcArthur K, Whitehead LW, Heddleston JM, Li L, Padman BS, Oorschot V, et al. BAK\u002FBAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis. Science. 2018;359(6378):eaao6047.\nYu CH, Davidson S, Harapas CR, Hilton JB, Mlodzianoski MJ, Laohamonthonkul P, et al. TDP-43 Triggers Mitochondrial DNA Release via mPTP to Activate cGAS\u002FSTING in ALS. Cell. 2020;183(3):636-49 e18.\nCassidy-Stone A, Chipuk JE, Ingerman E, Song C, Yoo C, Kuwana T, et al. Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax\u002FBak-dependent mitochondrial outer membrane permeabilization. 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biological function of lncRNA ELF3-AS1 remains largely unknown in cancers. The cause of SNAI2 overexpression in tumor metastasis remains largely unclear. The molecular mechanisms underlying the high co-expression of antisense lncRNAs and adjacent protein-coding genes remains unclear. RNA-seq, CHIP and dual-luciferase reporter assay were performed to identify lncRNAs regulated by SNAI2. MicroRNA-seq and RNA-seq studies were conducted to reveal the biological function of ELF3-AS1 in GC. RNA pulldown and CHIRP assays were conducted to identify the protein that interacts with ELF3-AS1. A total of 123 lncRNAs were identified to be regulated by SNAI2 in GC by RNA sequencing. The ELF3 gene and antisense lncRNA ELF3-AS1 were both transcriptionally repressed by SNAI2 or SNAI1. Down-regulation of ELF3-AS1 and ELF3 predicted poor prognosis in GC. Nuclear localized lncRNA ELF3-AS1 negatively regulated GC cell cycle progression via suppressing G1\u002FS transition and histone synthesis. ELF3-AS1 mainly inhibited GC metastasis by repressing SNAI2 signaling. Additionally, ELF3-AS1 modulated ELF3 mRNA stability by RNA-RNA interaction. The RNA duplexes formed by ELF3 mRNA and lncRNA ELF3-AS1 directly interacted with the double-stranded RNA (dsRNA) binding protein complex ILF2\u002FILF3 (NF45\u002FNF90). In turn, the ILF2\u002FILF3 complex dynamically regulated the expression of ELF3-AS1 and ELF3 by affecting the dsRNA stability. The SNAI2-ELF3-AS1 feedback loop regulates ELF3 expression at transcriptional and post-transcriptional levels and drives gastric cancer metastasis by maintaining SNAI2 overexpression. The ILF2\u002FILF3 complex plays a critical role in regulating dsRNA stability. In addition, our work provides a direct evidence that head-to-head antisense lncRNAs can share promoters with neighboring coding genes, which make their expression subject to similar transcriptional regulation, leading to high co-expression.",{"EN":2933},"LncRNA ELF3-AS1 inhibits gastric cancer by forming a negative feedback loop with SNAI2 and regulates ELF3 mRNA stability via interacting with ILF2\u002FILF3 complex",{"VOID":2935},"Siegel RL, Miller KD, Fuchs HE, Jemal A. Cancer Statistics, 2021. Ca-Cancer J Clin. 2021;71(1):7–33.\nSakai H, Kawakami H, Teramura T, Onodera Y, Somers E, Furuuchi K, et al. Folate receptor alpha increases chemotherapy resistance through stabilizing MDM2 in cooperation with PHB2 that is overcome by MORAb-202 in gastric cancer. Clin Transl Med. 2021;11(6)e454.\nWang XH, Jiang ZH, Yang HM, Zhang Y, Xu LH. Hypoxia-induced FOXO4\u002FLDHA axis modulates gastric cancer cell glycolysis and progression. Clin Transl Med. 2021;11(1):e279.\nWang J, Zhang M, Hu X, She J, Sun R, Qin S, et al. miRNA-194 predicts favorable prognosis in gastric cancer and inhibits gastric cancer cell growth by targeting CCND1. FEBS Open Bio. 2021;11(7):1814–26.\nVan Cutsem E, Sagaert X, Topal B, Haustermans K, Prenen H. Gastric cancer. Lancet. 2016;388(10060):2654–64.\nGotoda T, Yanagisawa A, Sasako M, Ono H, Nakanishi Y, Shimoda T, et al. Incidence of lymph node metastasis from early gastric cancer: estimation with a large number of cases at two large centers. Gastric Cancer. 2000;3(4):219–25.\nMervic L. Time course and pattern of metastasis of cutaneous melanoma differ between men and women. Plos One. 2012;7(3):e32955.\nChen Q, Ge X, Zhang Y, Xia H, Yuan D, Tang Q, et al. Plasma miR-122 and miR-192 as potential novel biomarkers for the early detection of distant metastasis of gastric cancer. Oncol Rep. 2014;31(4):1863–70.\nWang J, Zhang M, Hu X, She J, Sun R, Qin S, et al. MiRNA-194 predicts favorable prognosis in gastric cancer and inhibits gastric cancer cell growth by targeting CCND1: FEBS Open Bio; 2021.\nLi D, Cheng P, Wang J, Qiu X, Zhang X, Xu L, et al. IRF6 is directly regulated by ZEB1 and ELF3, and predicts a favorable prognosis in gastric cancer. Front Oncol. 2019;9:220.\nQin S, Wang Z, Huang C, Huang P, Li D. Serine protease PRSS23 drives gastric cancer by enhancing tumor associated macrophage infiltration via FGF2. Front Immunol. 2022;13.\nFan HJ, Wang XX, Li WY, Shen MH, Wei Y, Zheng HQ, et al. ASB13 inhibits breast cancer metastasis through promoting SNAI2 degradation and relieving its transcriptional repression of YAP. Genes Dev. 2020;34(19-20):1359–72.\nLi WY, Shen MH, Jiang YZ, Zhang RN, Zheng HQ, Wei Y, et al. Deubiquitinase USP20 promotes breast cancer metastasis by stabilizing SNAI2. Genes Dev. 2020;34(19-20):1310–5.\nDu F, Li XW, Feng WB, Qiao CY, Chen J, Jiang MZ, et al. SOX13 promotes colorectal cancer metastasis by transactivating SNAI2 and c-MET. Oncogene. 2020;39(17):3522–40.\nOlmeda D, Montes A, Moreno-Bueno G, Flores JM, Portillo F, Cano A. Snai1 and Snai2 collaborate on tumor growth and metastasis properties of mouse skin carcinoma cell lines. Oncogene. 2008;27(34):4690–701.\nFan L, Lei H, Zhang S, Peng Y, Fu C, Shu G, et al. Non-canonical signaling pathway of SNAI2 induces EMT in ovarian cancer cells by suppressing miR-222-3p transcription and upregulating PDCD10. Theranostics. 2020;10(13):5895.\nPeng L, Fu J, Chen Y, Ming Y, He H, Zeng S, et al. Transcription factor SNAI2 exerts pro-tumorigenic effects on glioma stem cells via PHLPP2-mediated Akt pathway. Cell Death Dis. 2022;13(6):1–9.\nLi DD, Wang JJ, Zhang MX, Hu XH, She JJ, Qiu XM, et al. LncRNA MAGI2-AS3 Is Regulated by BRD4 and Promotes Gastric Cancer Progression via Maintaining ZEB1 Overexpression by Sponging miR-141\u002F200a. Mol Ther-Nucl Acids. 2020;19:109–23.\nLi D, Xu M, Wang Z, Huang P, Huang C, Chen Z, et al. The EMT-induced lncRNA NR2F1-AS1 positively modulates NR2F1 expression and drives gastric cancer via miR-29a-3p\u002FVAMP7 axis. Cell Death Dis. 2022;13(1):1–10.\nLi D, She J, Hu X, Zhang M, Sun R, Qin S. The ELF3-regulated lncRNA UBE2CP3 is over-stabilized by RNA–RNA interactions and drives gastric cancer metastasis via miR-138-5p\u002FITGA2 axis. Oncogene. 2021;40(35):5403–15.\nDavis MC, Kesthely CA, Franklin EA, MacLellan SR. The essential activities of the bacterial sigma factor. Can J Microbiol. 2017;63(2):89–99.\nAli MM, Akhade VS, Kosalai ST, Subhash S, Statello L, Meryet-Figuiere M, et al. PAN-cancer analysis of S-phase enriched lncRNAs identifies oncogenic drivers and biomarkers. Nat Commun. 2018;9(1):883.\nStatello L, Ali MM, Reischl S, Mahale S, Kosalai ST, Huarte M, et al. The DNA damage inducible lncRNA SCAT7 regulates genomic integrity and topoisomerase 1 turnover in lung adenocarcinoma. 2021;3(1):zcab002.\nZhang Z, Nong L, Chen M-L, Gu X-L, Zhao W-W, Liu M-H, et al. LncRNA ELF3-AS1 Promotes Non-Small Cell Lung Cancer Cell Invasion and Migration by Downregulating miR-212. Cancer Biother Radiopharm. 2022;37(2):119–24.\nLuo S, Lu JY, Liu L, Yin Y, Chen C, Han X, et al. Divergent lncRNAs Regulate Gene Expression and Lineage Differentiation in Pluripotent Cells. Cell Stem Cell. 2016;18(5):637–52.\nChen LL. Linking Long Noncoding RNA Localization and Function. Trends Biochem Sci. 2016;41(9):761–72.\nSatyanarayana A, Hilton MB, Kaldis P. p21 inhibits Cdk1 in the absence of Cdk2 to maintain the G1\u002FS phase DNA damage checkpoint. Mol Biol Cell. 2008;19(1):65–77.\nFiaschi-Taesch NM, Salim F, Kleinberger J, Troxell R, Cozar-Castellano I, Selk K, et al. Induction of Human beta-Cell Proliferation and Engraftment Using a Single G1\u002FS Regulatory Molecule, cdk6. Diabetes. 2010;59(8):1926–36.\nWen X, Liu X, Mao YP, Yang XJ, Wang YQ, Zhang PP, et al. Long non-coding RNA DANCR stabilizes HIF-1alpha and promotes metastasis by interacting with NF90\u002FNF45 complex in nasopharyngeal carcinoma. Theranostics. 2018;8(20):5676–89.\nGuan DY, Altan-Bonnet N, Parrott AM, Arrigo CJ, Li Q, Khaleduzzaman M, et al. Nuclear factor 45 (NF45) is a regulatory subunit of complexes with NF90\u002F110 involved in mitotic control. Mol Cell Biol. 2008;28(14):4629–41.\nOh SC, Sohn BH, Cheong JH, Kim SB, Lee JE, Park KC, et al. Clinical and genomic landscape of gastric cancer with a mesenchymal phenotype. Nat Commun. 2018;9(1):1777.\nCristescu R, Lee J, Nebozhyn M, Kim KM, Ting JC, Wong SS, et al. Molecular analysis of gastric cancer identifies subtypes associated with distinct clinical outcomes. Nat Med. 2015;21(5):449–56.\nBartl J, Zanini M, Bernardi F, Forget A, Blümel L, Talbot J, et al. The HHIP-AS1 lncRNA promotes tumorigenicity through stabilization of dynein complex 1 in human SHH-driven tumors. Nat Commun. 2022;13(1):1–15.\nBryzghalov O, Szczesniak MW, Makalowska I. Retroposition as a source of antisense long non-coding RNAs with possible regulatory functions. Acta Biochim Pol. 2016;63(4):825–33.\nMahale S, Setia M, Prajapati B, Subhash S, Yadav MP, Thankaswamy Kosalai S, et al. HnRNPK maintains single strand RNA through controlling double-strand RNA in mammalian cells. Nat Commun. 2022;13(1):1–20.\nZheng H, Kang Y. Multilayer control of the EMT master regulators. 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