MFAP2 Promotes the Proliferation of Cancer Cells and Is Associated With a Poor Prognosis in Hepatocellular Carcinoma

Xiang Zhu1,2, Ye Cheng1, Fan Wu1, Haoyao Sun3, Wubin Zheng1, Wei Jiang1, Junfeng Shi4, Shijie Ma5, Hongyong Cao1
1Department of General Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, People's Republic of China
2Department of General Surgery, The East District of Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu, People's Republic of China
3Department of Radio-Oncology, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu, People's Republic of China
4Department of Oncology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, People’s Republic of China
5Department of Gastroenterology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Nanjing, People's Republic of China

Tóm tắt

Backgrounds: Microfibril-associated protein 2 (MFAP2) is an extracellular matrix protein that regulates the function of microfibrils by interacting with fibrillin. MFAP2 has been reported to play an important role in metabolic diseases and has been shown to be significantly overexpressed in head and neck squamous cell carcinoma and Hepatocellular carcinoma (HCC). However, the molecular function and prognostic value of MFAP2 have never been reported in HCC or other tumors. Methods: In the present study, expression characteristics of MFAP2 in HCC, its influence on the development of HCC, as well as its function and potential mechanism in HCC were verified by Quantitative reverse transcription-polymerase chain reaction, bioinformatics data mining and in vitro cell experiments. Results: MFAP2 was prominently high-expressed in HCC and associated with cancer stages. HCC patients with higher MFAP2 expression displayed lower overall survival (OS) and disease-specific survival(DSS), while there was no significant difference in recurrence-free survival (RFS). In vitro experiments showed that downregulation of MFAP2 inhibited proliferation, migration level of HCC cells. Transcription factors, DNA methyltransferases, immune factors may interact with MFAP2 mRNA to promote tumor progression in HCC. Conclusion: These findings suggest that MFAP2 may play a key role in the development of HCC. Therefore, MFAP2 may be a valuable prognostic marker and an effective anticancer target in HCC.

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