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

Authors :
Xiang Zhu MD
Ye Cheng MD
Fan Wu MD
Haoyao Sun MD
Wubin Zheng MD
Wei Jiang MD
Junfeng Shi PhD
Shijie Ma MD
Hongyong Cao MD
Source :
Technology in Cancer Research & Treatment, Vol 19 (2020)
Publication Year :
2020
Publisher :
SAGE Publishing, 2020.

Abstract

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.

Details

Language :
English
ISSN :
15330338
Volume :
19
Database :
Directory of Open Access Journals
Journal :
Technology in Cancer Research & Treatment
Publication Type :
Academic Journal
Accession number :
edsdoj.591aa69ab53242468b94ea05b5746034
Document Type :
article
Full Text :
https://doi.org/10.1177/1533033820977524