CircLATS2 Regulates miR-520a-3p/E2F7/p-VEGFR2 Signaling Pathway to Promote Hepatocellular Carcinoma Progression and Angiogenesis

Objective. To investigate the effect of circLATS2 on the progression and angiogenesis of hepatocellular carcinoma and its molecular mechanism. Methods. The expression of circLATS2 in hepatocellular carcinoma was detected by qRT-PCR. The StarBase database was used to predict the potential miRNA, and the combination of the above was cytological verified by luciferase reporter gene assay and RNA pull down. The potential target genes of miRNA were predicted by TargetScan, verified by the above experiments, and the influence of circLATS2 on its expression was determined. The biological function of circLATS2 was investigated by in vitro and in vivo experiments. The effects of miRNA and target genes on the malignant behavior of HCC cells were determined by the reverse experiment. Results. circLATS2 was highly expressed in HCC and was positively correlated with tumor size and tumor stage. miR-520a-3p was sponged by circLATS2 and was low expressed in HCC tissues. As the target gene of miR-520a-3p, the expression level of E2F7 is affected by circLATS2. In vitro experiments showed that circLATS2 knockdown inhibited the proliferation, clone formation, migration, and invasion ability of hepatocellular carcinoma cells. In vivo knockdown of circLATS2 inhibits the proliferation of HCC cells, while overexpression of circLATS2 promotes the proliferation of HCC cells. Overexpression of miR-520a-3p and E2F7 knockdown reversed the role of circLATS2 in promoting malignant behavior of HCC cells and affected phosphorylation of VEGFR2. Conclusion. CircLATS2 promotes the progression of HCC by regulating miR-520a-3p/E2F7/P-VEGFR2 signaling pathway.