Dihydromyricetin Reduces TGF-β Via P53 Activation-dependent Mechanism in Hepatocellular Carcinoma HepG2 Cells

Natural antineoplastic drug development is crucial to treatment of clinical oncology. Di-hydromyricetin, a bioactive flavonoid compound was extracted from the stems and leaves of Ampelopsis grossedentata. It exhibited anticancer activity and induced apoptosis in human hepatocellular carcinoma cells according to our previous studies. In this study, we demonstrated that DHM could significantly inhibit proliferation and induce apoptosis in HepG2 cells with MTT and Flow Cytometry methods. It is very interesting that we found DHM could regulate TGF-beta signal pathway and which has a crosstalk with P53, Smad3 and P-Smad2/3 proteins. Meanwhile, we confirmed that DHM showed antitumor activity by regulating the activation of the p53-dependent pathways (MDM2, P-MDM2, BAX and Bcl-2). These findings defined and supported a novel mechanism that DHM could induce cell apoptosis by reducing TGF-beta via p53 signal pathway in HepG2 cells.