Objective To detect the apoptosis effects of dioscin in HepG2 cells and its possible antihepatocellular carcinoma mechanisms. Methods HepG2 human hepatocellular carcinoma cells were exposed to 0. 25,0. 5, 1, 2, 4, 6, or 8 μmol / L dioscin, and cell proliferation was measured via MTT assay. The half-maximal inhibitory concentration ( IC50) was calculated with the software. A scratch test was used to analyze cell migration ability. Western blot was employed to evaluate the expression of apoptosis and Wnt / β-catenin-pathway-related proteins. Results Compared with the control group, the dioscin-treated HepG2 cells’ proliferation was significantly more inhibited, and the inhibition increased in a time- and dose-dependent manner (P<0. 01) . HepG2 cells showed morphological characteristics of apoptosis after they were treated with 1 μmol / L or 2 μmol / L dioscin. The scratch test indicated that the migration distance of HepG2 cells was remarkably reduced when treated with dioscin. In the Western blot experiment, the expression levels of Caspase3 and cleaved Caspase-3 were visibility up-regulated, while those of Bcl-2 and β-catenin were significantly down-regulated when the cells were treated with dioscin for 24 h (P<0. 05, P<0. 01) . When LiCl reagent was added to the HepG cells to activate the Wnt / β-catenin signaling pathway, the expression levels of Wnt1 and β-catenin were remarkably increased compared with those of the control group (P<0. 01) . Compared with the LiCl group, the LiCl + DIO group’ s expression of Wnt1, β-catenin, and GSK-3β was significantly decreased ( P<0. 01) . Conclusions DIO can promote the apoptosis of HepG2 cells by inhibiting β-catenin protein expression and thereby down-regulating the Wnt / β-catenin signaling pathway. This inhibits apoptosis-related gene Bcl-2 expression, which leads to the induction of cell apoptosis. Therefore, DIO can have an anti-hepatocellular carcinoma effect.