LncRNAs play an important role in tumorigenesis and cancer progression in liver cancer. Although many lncRNAs have been reported, the role of MIR194-2HG and the underlying mechanism mediated by it are still largely unknown in HCC. This study aimed to investigate the biological role and mechanism of MIR194-2HG in liver cancer. Materials and Methods: The expression of MIR194-2HG was determined in liver cancer tissues and cells by RT-qPCR. The overall survival rate of MIR194-2HG was analyzed by Kaplan-Meier survival analysis. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, and Transwell assays were carried out to detect cell migration and invasion. Western blotting was used to quantify the levels of all proteins. The regulatory mechanism of the MIR194-2HG/miR-1207-5p/TCF19 axis in liver cancer was investigated by dual-luciferase activity reporter assay, Kaplan-Meier survival analysis, and Western blotting. Results: MIR194-2HG was upregulated in liver cancer tissues and cell lines. Liver cancer patients with higher expression of MIR194-2HG revealed poor overall survival compared with those who had lower expression of MIR194-2HG. MIR194-2HG promoted the proliferation, migration, and invasion of HepG2 and Huh7 cells by acting as a ceRNA mechanism for the miR-1207-5p/TCF19 axis to activate the Wnt/β-catenin signaling pathway. Conclusion: MIR194-2HG acts in an oncogenic role and activates the Wnt/β-catenin signaling pathway via a miR-1207-5p/TCF19 axis-mediated mechanism, which provides a novel avenue for diagnostic or therapeutic interventions in liver cancer.

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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.

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