Ginsenoside Rg3 inhibits the biological activity of SGC‐7901

AIM: To explore the suppressive effects of ginsenoside Rg3 on the biological activities of gastric cancer and the mechanisms responsible therein, by conducting an in vitro study. MATERIALS AND METHODS: SGC‐7901 gastric cancer cells were divided into NC, DMSO, Gin‐Low (10 mg/L), Gin‐Middle (20 mg/L), and Gin‐High (40 mg/L) groups. Using MTT, flow cytometry, transwell, and wound‐healing assays, the cell biological activities in the different groups were evaluated; the protein expression levels of PTEN, p‐PI3K, AKT, and P53 were measured by Western blot assay, and p‐PI3K nuclear volume was evaluated by immunofluorescence. RESULTS: The SGC‐7901 cell proliferation rate was depressed significantly, and cell apoptosis increased significantly while cells were arrested in the G1 phase (p < .05) with ginsenoside Rg3 treatment in a dose‐dependent manner (p < .05). Meanwhile, the SGC‐7901 cell invasion number and wound‐healing rate of ginsenoside Rg3‐treated groups were significantly downregulated compared with those of the NC group, also in a dose‐dependent manner (p < .05). PTEN and P53 protein expression levels were significantly increased, and p‐PI3K and AKT protein expression levels were significantly depressed in ginsenoside Rg3‐treated groups in a dose‐dependent manner (p < .05). CONCLUSION: Ginsenoside Rg3 suppresses gastric cancer via regulation of the PTEN/p‐PI3K/AKT pathway.