Retracted: MicroRNA‐519a promotes proliferation and inhibits apoptosis of hepatocellular carcinoma cells by targeting FOXF2

Autor: Junwei Shao, Jun Cao, Yong Liu, Hongliang Mei, Yang Zhang, Weitian Xu
Jazyk: angličtina
Rok vydání: 2015
Předmět:
Zdroj: FEBS Open Bio, Vol 5, Iss 1, Pp 893-899 (2015)
Druh dokumentu: article
ISSN: 2211-5463
DOI: 10.1016/j.fob.2015.10.009
Popis: Recent studies report that microRNA‐519a (miR‐519a) is a novel oncomir, which facilitates the onset and progression of human cancers. However, the clinical significance of miR‐519a and its functional role and underlying mechanisms in hepatocellular carcinoma (HCC) are poorly investigated. In the present study, elevated expression of miR‐519a was observed in HCC tissues compared with adjacent non‐tumor tissues. The increased level of miR‐519a expression was significantly correlated with adverse clinical features of HCC including hepatitis B virus (HBV) infection, large tumor size, cirrhosis and advanced tumor‐node‐metastasis tumor stage. Furthermore, high expression of miR‐519a was prominently associated with a poorer 5‐year overall survival and recurrence‐free survival of HCC patients. Gain‐ and loss‐of function experiments showed that miR‐519a overexpression enhanced proliferation and reduced apoptosis of Huh7 cells. By contrast, miR‐519a knockdown inhibited SMMC‐7721 cell proliferation and induced apoptosis. Importantly, up‐regulation of miR‐519a reduced the expression of FOXF2 mRNA and protein in Huh7 cells, while down‐regulation of miR‐519a resulted in increased expression of FOXF2 in SMMC‐7721 cells. An inverse correlation between mRNA levels of miR‐519a and FOXF2 was observed in HCC tissues. Thus, Forkhead box F2 (FOXF2) was identified as a downstream target of miR‐519a in HCC. Mechanistically, the effects of miR‐519a knockdown on SMMC‐7721 cells were abrogated by FOXF2 repression. In conclusion, miR‐519a is a novel prognostic predictor for HCC patients and it may potentiate proliferation and inhibits apoptosis of HCC cells by targeting FOXF2.
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