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Ginsenoside Rg3 inhibits the biological activity of SGC-7901
Qing Yang1, Ning Cai1, Daobiao Che1
1Department of Hospital Pharmacy Suqian First Hospital Suqian China.
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.
Insights
Ginsenoside Rg3 effectively suppresses gastric cancer cell growth and invasion. It also promotes apoptosis by regulating the PTEN/p-PI3K/AKT pathway, offering a potential therapeutic strategy.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Gastric cancer remains a significant global health challenge.
- Ginsenoside Rg3, a natural compound, has shown potential anti-cancer properties.
- Understanding its precise mechanisms in gastric cancer is crucial for therapeutic development.
Purpose of the Study:
- To investigate the inhibitory effects of ginsenoside Rg3 on gastric cancer cell biological activities.
- To elucidate the underlying molecular mechanisms of ginsenoside Rg3 action in vitro.
- To evaluate the impact of ginsenoside Rg3 on cell proliferation, apoptosis, invasion, and key signaling pathways.
Main Methods:
- In vitro study using SGC-7901 gastric cancer cells.
- Treatment with varying concentrations of ginsenoside Rg3 (10, 20, 40 mg/L).
- Assays included MTT, flow cytometry, Transwell, wound-healing, Western blot, and immunofluorescence to assess cell viability, apoptosis, invasion, migration, and protein expression (PTEN, p-PI3K, AKT, P53).
Main Results:
- Ginsenoside Rg3 significantly inhibited SGC-7901 cell proliferation and induced apoptosis in a dose-dependent manner.
- Cell cycle arrest at the G1 phase was observed.
- Invasion and wound-healing rates were significantly reduced, with a dose-dependent effect.
- Upregulation of PTEN and P53 protein expression, and downregulation of p-PI3K and AKT were noted.
Conclusions:
- Ginsenoside Rg3 demonstrates significant suppressive effects on gastric cancer cell proliferation, invasion, and migration.
- The compound exerts its anti-cancer effects through the regulation of the PTEN/p-PI3K/AKT signaling pathway.
- Ginsenoside Rg3 represents a promising therapeutic agent for gastric cancer treatment.
