miR-29a overexpresion induces apoptosis through targeting VEGF in hepatocellular carcinoma

Abstract

Background : This study aimed to explore the role of miR-29a in hepatocellular carcinoma (HCC) cells. Further, to confirm whether miR-29a targetes vascular endothelial growth factor (VEGF) in HCC cells. Methods: Cell counting Kit-8 (CCK8) and clone formation assay were used to analyze the proliferation of HCC cells. Flow cytometry was performed to analyze the apoptosis and cell cycle of HCC cells. Western blot was used to analyze the expression of Bax, B-cell lymphoma-2 (Bcl-2), cyclin dependent kinase 4 (CDK4), CyclinD1, Retinoblastoma (Rb), p53 and myeloid cell leukemia-1 (MCL1). The targeting relations between miR-29a and VEGF was measuered by dual luciferase assay. Results : Overexpression of miR-29a could distinctly inhibit the proliferation and promote apoptosis of HCC cells. Overexpression of miR-29a obviously up-regulated the expressions of Bax and Rb, and reduced the expressions of CDK4, Bcl-2, Cyclin D1, p53, MCL1 and VEGF in HCC cells. Dual luciferase assay proved that VEGF was the target of miR-29a. Rescue experiments showed that miR-29a targeted VEGF to regulate the proliferation and apoptosis in HCC cells. Conclusions : These results indicated overexpression of miR-29a inhibited the HCC cells proliferation through targeting VEGF.