Berberine inhibits angiogenic potential of Hep G2 cell line through VEGF down‐regulation in vitro

Abstract

Berberine, an herbal alkaloid, has been reported to have promotion potential of apoptosis and anticancer effect on a variety of human tumor cells. To obtain more specific understanding of those consequences of berberine on hepatocellular carcinoma (HCC) and the tumor microenvironment, we conducted in vitro experiments to investigate the inhibitory effect of berberine on tumor-induced angiogenesis using HCC cells and human umbilical vein endothelial cells (HUVECs). Human umbilical vein endothelial cell growth was quantified with the CCK-8 cell proliferation assay; cell migration was observed with a Boyden chamber (Transwell, Corning, Lowell, MA, USA), and angiogenesis was assessed by endothelial tube formation in Matrigel in vitro. In addition, VEGF level was determined by ELISA and VEGF mRNA expression by RT-PCR. Berberine inhibited the capacity of HCC to stimulate HUVEC's proliferation, migration and endothelial tube formation, suggesting that berberine could influence the cross-talk between the HCC cell and vascular endothelial cells. These results demonstrate berberine's antiangiogenesis property and its clinical potential as an inhibitor of tumor angiogenesis. Subsequently analyses reveal that berberine prevents secretion of VEGF from HCC and down-regulates VEGF mRNA expression. These findings strongly suggest that berberine is a potential antiangiogenic agent and a promising antitumor drug for HCC.