Các con đường tín hiệu liên quan đến lncRNA MALAT1 trong u xương Osteosarcoma

Clinical and Translational Oncology - Tập 25 - Trang 21-32 - 2022
Maryam Farzaneh1, Sajad Najafi2, Omid Anbiyaee3, Shirin Azizidoost4, Seyed Esmaeil Khoshnam5
1Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
2Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3School of Medicine, Cardiovascular Research Center, Nemazi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran
4Atherosclerosis Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
5Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Tóm tắt

Osteosarcoma (OS) là một dạng ung thư xương phổ biến và ác tính, ảnh hưởng đến trẻ em và thanh thiếu niên. OS được xác định bởi sự biệt hóa tạo xương và sự di căn. Tuy nhiên, cơ chế phân tử chính xác của sự phát triển và tiến triển của OS vẫn chưa được làm rõ. Gần đây, lncRNA (RNA không mã hóa dài) đã được chứng minh là điều chỉnh sự tăng sinh và kháng thuốc của OS. LncRNA dài hơn 200 nucleotide và đại diện cho các ứng dụng rộng rãi trong quá trình xử lý pre-mRNA và bệnh sinh của các bệnh ở người. Dịch mã adenocarcinoma ở phổi liên quan đến di căn – transcript-1 (MALAT1) là một lncRNA nổi tiếng, được biết đến như là một chất điều chỉnh phiên mã và dịch mã. Biểu hiện bất thường của MALAT1 đã được chứng minh trong một số loại ung thư ở người. Mức độ cao của MALAT1 liên quan đến sự phát triển và ác tính của tế bào OS thông qua việc nhắm mục tiêu vào một số con đường tín hiệu và miRNA. Do đó, MALAT1 có thể là một phương pháp thích hợp cho việc chẩn đoán và điều trị OS. Trong bài viết này, chúng tôi sẽ tóm tắt vai trò của lncRNA MALAT1 trong bệnh sinh của OS.

Từ khóa

#Osteosarcoma #lncRNA #MALAT1 #di căn #kháng thuốc #ung thư xương

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