Dihydromyricetin Reduced Bcl-2 Expression via p53 in Human Hepatoma HepG2 Cells

Abstract

Dihydromyricetin (DHM) is a major active ingredient of flavonoids compounds. It exhibited anticancer activity and induced apoptosis in human hepatocellular carcinoma HepG2 cells according to our previous data. In this study, we investigated whether p53 is involved in DHM-triggered viability inhibition and apoptosis induction in cancer cells. MTT [3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide] assay was employed to evaluate the viability of HepG2 cells after DHM treatment. Meanwhile, p53 small interfering RNA (siRNA) was adopted to silence p53 expression. Protein level of p53 and Bax/Bcl-2 were evaluated by western blot analysis. Cell counting assay showed that DHM inhibited HepG2 cell growth effectively in a time- and dose-dependent manner. P53 expression was significantly increased after DHM treatment, whereas Bcl-2 was reduced potently. Furthermore, after co-treatment with Pifithrin-α (PFT-α, p53 inhibitor), Bcl-2 expression was reversed. The expression of Bax was no significant change, which was also observed after p53 silence. These findings defined and supported a novel function that DHM could induce human hepatocellular carcinoma HepG2 cells apoptosis by up-regulating Bax/Bcl-2 expression via p53 signal pathway.

Dihydromyricetin induces cell apoptosis via a p53-related pathway in AGS human gastric cancer cells

“…We also demonstrated that at concentrations of 25 to 100 μM, DHM inhibited gastric cancer cell (AGS) proliferation and induced cell apoptosis. The antitumor effects of DHM were consistent with previous reports using liver cancer cells (Wu et al, 2013;Zhang et al, 2014). These results suggested that DHM is a potent antitumor compound that can regulate specific genes responsible for tumor cell proliferation and apoptosis.…”

“…Recent reports also demonstrate potent anticancer activity of DHM (Wu et al, 2013;Zhang et al, 2014). Specifically, DHM has been found to inhibit cell proliferation in human hepatoma cells via p53-related pathways (Wu et al, 2013).…”

Targeting of growth factors in the treatment of hepatocellular carcinoma: The potentials of polysaccharides

“…Dihydromyricetin (DHM) is the active component in extracts of Ampelopsis grossedentata. The principal anticancer mechanism of DHM is via the induction of p53-dependent apoptosis (73)(74)(75). A previous study demonstrated that DHM enhances chemosensitivity to nedaplatin (a platinum-containing chemotherapeutic drug) by activating the p53/B-cell lymphoma 2 (Bcl-2) signaling pathway, which resulted in mitochondrial dysfunction and induced cell death and growth inhibition in HCC cells (76).…”

Dihydromyricetin Induces Apoptosis by Reducing TGF-β via P53 Activation in HepG2 Cells

“…It was reported that DHM could promote hepatocellular carcinoma apoptosis via the P53 activationdependent pathway [3,4]. Meanwhile it could induce Hep G2 cells autophagy involved inhibition of m-TOR [5].…”