Open AccessGinsenoside Rg3 inhibits the biological activity of SGC‐7901
Author(s) -
Yang Qing,
Cai Ning,
Che Daobiao,
Chen Xing,
Wang Dongliang
Publication year - 2020
Publication title -
food science and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.614
H-Index - 27
ISSN - 2048-7177
DOI - 10.1002/fsn3.1707
Subject(s) - pten , pi3k/akt/mtor pathway , protein kinase b , ginsenoside , western blot , apoptosis , cell cycle , chemistry , flow cytometry , cell growth , mtt assay , cell , pharmacology , cancer research , microbiology and biotechnology , medicine , biology , biochemistry , pathology , ginseng , alternative medicine , gene
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.