Long non-coding RNA COX7C-5 promotes hepatocellular carcinoma progression via miR-581/ZEB2 axis

Long non-coding RNAs (lncRNA) play crucial roles in hepatocellular carcinoma (HCC) progression. However, the functional roles of lncRNAs in HCC still remain largely unknown. Our study aimed to investigate the biological function and potential molecular mechanism of lnc-COX7C-5 in HCC. Here, we show that Lnc-COX7C-5 was significantly upregulated in HCC tissues, which was correlated with poor prognosis in HCC patients. Lnc-COX7C-5 positively regulated proliferation, migration, and invasion of HCC cells. Mechanistically, lnc-COX7C-5 function as a competing endogenous RNA (ceRNA) for miR-581 in HCC cells. Over-expression or knockdown of miR-581 could alter cell phenotypes caused by Lnc-COX7C-5 in HCC. Further investigations indicated that ZEB2 was demonstrated as a downstream target of miR-581. In mouse model, over-expression of Lnc-COX7C-5 facilitate lung metastasis of HCC. Collectively, Lnc-COX7C-5 promote HCC tumorigenesis and progression by targeting the miR-581/ZEB2 axis. Lnc-COX7C-5 may be a potential therapeutic target for HCC.

Automated summary

This study reveals that lnc-COX7C-5 is upregulated in HCC tissues and associated with poor prognosis. Lnc-COX7C-5 functions as a ceRNA for miR-581 in HCC cells. ZEB2 is identified as a downstream target of miR-581. In a mouse model, overexpression of lnc-COX7C-5 promotes lung metastasis in HCC.