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It is known that lncRNA CASC11 promotes the development of gastric cancer. Our study was carried out to investigate the possible involvement of ncRNA CASC11 in hepatocellular carcinoma (HCC). In the present study, we found that CASC11 was up-regulated, while miR-188-5p was down-regulated in tumor tissues of HCC patients. CASC11 and miR-188-5p were not affected by HBV and HCV infections. Follow-up study showed that high levels of CASC11 were significantly correlated with poor survival. Expression levels of CASC11 and miR-188-5p were inversely correlated in tumor tissues. CASC11 overexpression mediated the down-regulation of miR-188-5p, while miR-188-5p overexpression failed to affect CASC11 expression. CASC11 overexpression led to promoted, while miR-188-5p overexpression led to inhibited proliferation of cells of HCC cell lines. CASC11 overexpression showed no significant effects on cancer cell migration and invasion. In addition, miR-188-5p overexpression attenuated the enhancing effects of CASC11 overexpression on cancer cell proliferation. Therefore, LncRNA CASC11 promoted cancer cell proliferation in HCC possibly by inhibiting miR-188-5p.

Long non-coding RNAs (lncRNAs) have emerged as key regulators in the development of hepatocellular carcinoma (HCC). In the present study, we explored the expression profile and biological role of lncRNA FEZF1-AS1 in HCC. We observed remarkable upregulation of FEZF1-AS1 in HCC tissues and cell lines, and high FEZF1-AS1 expression was correlated with aggressive phenotypes and poor prognosis of HCC patients. Furthermore, we found that FEZF1-AS1 knockdown markedly inhibited the proliferation of HCC cells by inducing cell cycle arrest. In addition, FEZF1-AS1 knockdown suppressed HCC tumor growth in vivo. Moreover, FEZF1-AS1 knockdown inhibited the migration and invasion of HCC cells through suppression of JAK2/STAT3 signaling-mediated epithelial-mesenchymal transition (EMT). In conclusion, the present study for the first time demonstrated that FEZF1-AS1 serves as an oncogenic lncRNA in human HCC and implicated FEZF1-AS1 as a valuable therapeutic target for HCC treatment.