LncRNA MINCR promotes the development of liver cancer by regulating microRNA-107/beta-catenin

Purpose: To investigate the level of long noncoding ribonucleic acid (IncRNA) MINCR in hepatocellular carcinoma (HCC), and to further investigate whether it can promote the development of HCC through modulating microRNA107/beta-catenin. Methods: MINCR level in 52 pairs of HCC tumor tissues as well as adjacent tissues and HCC cell lines was detected by quantitative real-time polymerise chain reaction (qRT-PCR). MINCR knockdown model was constructed using lentivirus in the carcinoma cell lines. Furthermore, cell counting kit8 (CCK-8), plate cloning and apoptosis assay were used to analyze the effect of MINCR on the biological function of HCC cells. Finally, cell recovery experiment was performed to explore its potential mechanism and the association between MINCR and microRNA-107/beta-catenin. Results: qPCR results showed that the level of MINCR in HCC was remarkably higher than that in adjacent tissues, and the difference was statistically significant. Compared with patients with low level of MINCR, patients with high level of MINCR had lower overall survival rate. Similarly, the cell proliferation ability of sh-MINCR group was remarkably decreased while the apoptosis ability was oppositely increased when compared with the short hairpin RNA (shRNA) group. In addition, studies have demonstrated that the levels of microRNA-107 and MINCR in HCC tissues were negatively related. In our study, dual-luciferase reporting assay verified that MINCR can be targeted by microRNA-107 through certain binding site. In addition, MINCR was confirmed to be able to further regulate the malignant progression of HCC through microRNA-107/beta-catenin. Conclusions: The level of MINCR was remarkably increased in HCC, which was associated with poor prognosis of HCC patients. Moreover, MINCR was capable of promoting the proliferation and inhibiting apoptosis of liver cancer cells via regulating microRNA-107/beta-catenin.