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The aim of the present study was to evaluate the antitumor mechanism of dihydromyricetin (DHM). Results showed that DHM significantly inhibited cell viability of HepG2 and Hep3B cells in a dose-dependent manner. DHM induced G2/M cell-cycle arrest in HepG2 and Hep3B cells by altering the expression of cell cycle proteins such as cyclin A, cyclin B1, Cdk1, p53, Cdc25c, p-Cdc25c Chk1 and Chk, which are critical for G2/M transition. Knockdown of p53 and Chk1 in HepG2 cells did not affect G2/M phase arrest caused by DHM. Furthermore, G2/M arrest induced by DHM can be disrupted by Chk2 siRNA. These findings indicate that DHM inhibits the growth of hepatocellular carcinoma (HCC) cells via G2/M phase cell cycle arrest through Chk1/Chk2/Cdc25C pathway. The present study identified effects of DHM in G2/M phase arrest in HCC and described detailed mechanisms of G2/M phase arrest by this agent, which may contribute to its overall cancer preventive efficacy in HCC.

Dihydromyricetin suppresses the proliferation of hepatocellular carcinoma cells by inducing G2/M arrest through the Chk1/Chk2/Cdc25C pathway