Ginsenoside Rg3 suppresses the proliferation of prostate cancer cell line PC3 through ROS-induced cell cycle arrest.

To investigate the potential antitumor effects of ginsenoside Rg3 in prostate cancer cells, the androgen-insensitive prostate cancer cell line PC3 was cultured and incubated with ginsenoside Rg3 . Cell number counts, cell proliferation assays and senescence-associated β-galactosidase (SA-β-gal) staining were performed to evaluate cell proliferation. The results demonstrated that ginsenoside Rg3 led to cell proliferation arrest; ginsenoside Rg3 decreased the number of cells and increased the positive SA-β-gal staining rate in PC3 cells. Cell cycle analysis by flow cytometry revealed that ginsenoside Rg3 interfered with the G1/S transition in PC3 cells. The mechanism involved in ginsenoside Rg3-induced cell proliferation arrest was then further investigated. This indicated that the level of reactive oxygen species (ROS) in PC3 cells was upregulated by ginsenoside Rg3 treatment. Furthermore, pretreatment with N-acetyl-L-cysteine, a scavenger of ROS, was able to reverse the effects on cell number and cell cycle arrest induced by ginsenoside Rg3 in PC3 cells. These results indicate that ginsenoside Rg3 exhibits anticancer effects on prostate cancer cells through ROS-mediated arrest of the cell cycle.