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Objective To observe the effects of daucosterol on the proliferation and apoptosis of human hepatocellular carcinoma HepG2 cells, and then to discuss its mechanism. Methods HepG2 cells were cultured in vitro，and then were divided into the daucosterol group and control group. In the daucosterol group， HepG2 cells were inoculated on 96-well plates by 5 X 105/mL, and different concentrations (25 μg/mL, 50 μg/mL, 100 μg/mL, 150 μg/mL and 200 μg/mL) of daucosterol were added, and we did not add any drugs to the control group. At 48 h after culture, CCK-8 was used to meas­ure cell proliferation inhibition. HepG2 cells were inoculated on 6-well plates by 5 X 105/mL, and 50 and 100 μg/mL daucosterol were added to the daucosterol group, and the control group was not added. At 48 h, flow cytometer was used to detected the apoptosis rate of HepG2 cells. Western blotting was performed to analyze the expression of apoptosis relative protein (Bax, Bcl-2) , and Wnt/p-catenin pathway relative protein (WNT3A, β-catenin) in the HepG2 cells. Results The inhibition rate of cell proliferation in each daucosterol subgroup was higher than that in the control group，and the inhibition rate of cell proliferation increased along with the concentrations (25，50，100，150 and 200 μg/mL) of daucosterol ( all P <0.05). The apoptosis rates of HepG2 cells in the 50 and 100 μg/mL daucosterol subgroups was higher than that of the control group，and the apoptosis rate of the 100 μg/mL daucosterol subgroup were higher than that of the 50 μg/mL dau­costerol subgroup (all P <0.05). The relative expression of Bax protein in the control group and the 50 and 100 μg/mL daucosterol subgroups increased successively， and the relative expression of Bcl-2，WNT3A， and β-catenin protein de­creased (all P <0.05). Conclusion Daucosterol inhibits the proliferation and promotes the apoptosis of HepG2 cells by inhibiting the Wnt/ p-catenin signaling pathway and regulating the expression of apoptosis-related proteins. [ABSTRACT FROM AUTHOR]