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Aberrant expression of long noncoding RNAs (lncRNAs) has been involved in progression of various human tumors including hepatocellular carcinoma (HCC). However, the role of lncRNAs in HCC has not fully explained. Our study aimed to investigate the biological function and potential molecular mechanism of Lnc-PAL2G4A-4 in HCC. Our study showed that Lnc-PLA2G4A-4 was significantly up-regulated in HCC tissues and higher Lnc-PLA2G4A-4 was remarkably related to tumor size, microvascular invasion and poor prognosis of HCC patients. Functionally, Lnc-PLA2G4A-4 positively regulated cell proliferation, invasion and migration in vitro, and facilitate lung metastasis of HCC in vivo. Mechanistically, Lnc-PLA2G4A-4 functioned as a competing endogenous RNA (ceRNA) to bind to miR-23b-3p and subsequently facilitated miR-23b-3p’s target gene versican (VCAN) expression in HCC cells. Over-expression of miR-23b-3p could reversed cell phenotypes caused by Lnc-PLA2G4A-4 in HCC and suppress the expression of versican by rescue analysis. Collectively, Lnc-PLA2G4A-4 promotes the progression of HCC via targeting miR-23b-3p/versican axis, which might be a potential biomarker and therapeutic target for HCC.

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.