Objective        To investigate the relationship between the anti-proliferation effect of ginsenoside Rg3 on colon cancer cells and Wnt/β-catenin signaling pathway.       Methods      Colon cancer cell line HCT116 were treated with different concentrations of ginsenoside Rg3

and the cells treated with DMSO were served as solvent control. Crystal violet staining and colony formation assay were applied to detect the anti-proliferation effect of ginsenoside Rg3 on HCT116 cells. Luciferase reporter assay was us

ed to measure the transcriptional activity of β-catenin/Tcf4 in HCT116 cells. The protein expression levels of β-catenin and c-Myc were detected by Western blotting. Immunofluorescent assay was used to observe the effect of ginsenoside Rg3 on nuclear translocation of β-catenin in SW480 cells.       Results      Ginsenoside Rg3 could inhibit the proliferation of HCT116 cells at the concentration of 60 μmol/L (vs control

P

0.05)

and this result was confirmed by colony formation assay in HCT116 cells. The transcriptional activity of β-catenin/Tcf4 in HCT116 cells was inhibited by ginsenoside Rg3 at the concentration of 25 μmol/L (vs control

P

0.05). The protein expression of c-Myc was down-regulated by ginsenoside Rg3

which had no obvious effect on the protein expression of β-catenin in HCT116 cells. The nuclear translocation of β-catenin was blocked by ginsenoside Rg3 in SW480 cells.        Conclusion        Ginsenoside Rg3 can inhibit the proliferation of colon cancer cells through inhibiting Wnt/β-catenin signal transduction by blocking the nuclear translocation of β-catenin.