Accumulating evidence have suggested that long non-coding RNAs (lncRNAs) act as a critical regulator in tumorgenesis. LncRNA KCNQ1OT1 (KCNQ1OT1) has been recently shown to be dysregulated in many cancers. This study was aimed to explore the biological role of KCNQ1OT1 in hepatocellular carcinoma (HCC). In our study, we first observed the expression level of KCNQ1OT1 was distinctly up-regulated in HCC tissues and cell lines compared with adjacent non-cancer tissues and normal liver cell line. And clinical results indicated that higher expression of KCNQ1OT1 was correlated with poor prognosis of patients with HCC. Next, functional studies revealed that knockdown of KCNQ1OT1 induced apoptosis and repressed proliferation, migration and invasion of HCC cells. In addition, knockdown of KCNQ1OT1 suppressed xenograft tumor growth in vivo. Mechanically, we found that KCNQ1OT1 can promote the expression of IGF1R by functioning as a competing endogenous RNA of miR-148a-3p. In conclusion, our results shown the oncogenic role of KCNQ1OT1 in HCC by regulating the miR-148a-3p/IGF1R axis and may provide a new insight and a potential therapeutic target for HCC.
Keywords: IGF1R; KCNQ1OT1; hepatocellular carcinoma; miR-148a-3p; tumor.