Ginsenoside Rg3 inhibits the biological activity of SGC‐7901
Abstract 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...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2020-08-01
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| Series: | Food Science & Nutrition |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/fsn3.1707 |
| _version_ | 1797661234061901824 |
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| author | Qing Yang Ning Cai Daobiao Che Xing Chen Dongliang Wang |
| author_facet | Qing Yang Ning Cai Daobiao Che Xing Chen Dongliang Wang |
| author_sort | Qing Yang |
| collection | DOAJ |
| description | Abstract 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. |
| first_indexed | 2024-03-11T18:41:28Z |
| format | Article |
| id | doaj.art-2c430552d9254830a8bf30406d698543 |
| institution | Directory Open Access Journal |
| issn | 2048-7177 |
| language | English |
| last_indexed | 2024-03-11T18:41:28Z |
| publishDate | 2020-08-01 |
| publisher | Wiley |
| record_format | Article |
| series | Food Science & Nutrition |
| spelling | doaj.art-2c430552d9254830a8bf30406d6985432023-10-12T12:06:11ZengWileyFood Science & Nutrition2048-71772020-08-01884151415810.1002/fsn3.1707Ginsenoside Rg3 inhibits the biological activity of SGC‐7901Qing Yang0Ning Cai1Daobiao Che2Xing Chen3Dongliang Wang4Department of Hospital Pharmacy Suqian First Hospital Suqian ChinaDepartment of Hospital Pharmacy Suqian First Hospital Suqian ChinaDepartment of Hospital Pharmacy Suqian First Hospital Suqian ChinaDepartment of Hospital Pharmacy Suqian First Hospital Suqian ChinaEmergency Department Suqian First Hospital Suqian ChinaAbstract 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.https://doi.org/10.1002/fsn3.1707AKTbiological activitiesgastric cancerginsenoside Rg3p‐PI3KPTEN |
| spellingShingle | Qing Yang Ning Cai Daobiao Che Xing Chen Dongliang Wang Ginsenoside Rg3 inhibits the biological activity of SGC‐7901 Food Science & Nutrition AKT biological activities gastric cancer ginsenoside Rg3 p‐PI3K PTEN |
| title | Ginsenoside Rg3 inhibits the biological activity of SGC‐7901 |
| title_full | Ginsenoside Rg3 inhibits the biological activity of SGC‐7901 |
| title_fullStr | Ginsenoside Rg3 inhibits the biological activity of SGC‐7901 |
| title_full_unstemmed | Ginsenoside Rg3 inhibits the biological activity of SGC‐7901 |
| title_short | Ginsenoside Rg3 inhibits the biological activity of SGC‐7901 |
| title_sort | ginsenoside rg3 inhibits the biological activity of sgc 7901 |
| topic | AKT biological activities gastric cancer ginsenoside Rg3 p‐PI3K PTEN |
| url | https://doi.org/10.1002/fsn3.1707 |
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