Yingying Chen 1 , Yuqiang Zhang 1 , Wei Song 1 , Ying Zhang 2 , Xiu Dong 3 , Mingqi Tan 1 . Show Affiliations »
Abstract
BACKGROUND: Ginsenoside Rh2 (Rh2) is a major biological component of ginseng that exerts antitumor activities in multiple cancers including Non-Small Cell Lung Cancers (NSCLCs). Rh2 also enhances the anti-tumor effects of various chemotherapy drugs including cisplatin at relatively low concentrations. Here, the mechanistic role of Rh2 in chemotherapy-treated NSCLCs will be investigated. METHODS: In this study, FACS, western blot and siRNA addition were used to analyze the role of Rh2 in cisplatin- treated lung adenocarcinoma A549 and H1299 cells. RESULTS: Subsequent observations indicated that Rh2 enhanced cisplatin-induced NSCLCs A549 and H1299 cells apoptosis. Cisplatin-induced productive autophagy was repressed by Rh2 in A549 cells. Rh2 also enhanced cisplatin cytotoxicity by elevating superoxide dismutase activity and repressing cisplatin-induced superoxide generation. Conversely, Rh2 was found to repress cisplatin-induced phosphorylation of epidermal growth factor receptor, phosphoinositide 3-kinase, protein kinase B, and autophagy. Cisplatin-induced Programmed Death- Ligand 1 (PD-L1) expression was repressed by Rh2 via the superoxide. CONCLUSION: These findings suggest that Rh2 enhanced the function of cisplatin by repressing superoxide generation, PD-L1 expression, and autophagy in lung adenocarcinoma cells. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
BACKGROUND: Ginsenoside Rh2 (Rh2 ) is a major biological component of ginseng that exerts antitumor activities in multiple cancers including Non-Small Cell Lung Cancers (NSCLCs ). Rh2 also enhances the anti-tumor effects of various chemotherapy drugs including cisplatin at relatively low concentrations. Here, the mechanistic role of Rh2 in chemotherapy-treated NSCLCs will be investigated. METHODS: In this study, FACS, western blot and siRNA addition were used to analyze the role of Rh2 in cisplatin - treated lung adenocarcinoma A549 and H1299 cells. RESULTS: Subsequent observations indicated that Rh2 enhanced cisplatin -induced NSCLCs A549 and H1299 cells apoptosis. Cisplatin -induced productive autophagy was repressed by Rh2 in A549 cells. Rh2 also enhanced cisplatin cytotoxicity by elevating superoxide dismutase activity and repressing cisplatin -induced superoxide generation. Conversely, Rh2 was found to repress cisplatin -induced phosphorylation of epidermal growth factor receptor , phosphoinositide 3-kinase, protein kinase B , and autophagy. Cisplatin -induced Programmed Death- Ligand 1 (PD-L1 ) expression was repressed by Rh2 via the superoxide . CONCLUSION: These findings suggest that Rh2 enhanced the function of cisplatin by repressing superoxide generation, PD-L1 expression, and autophagy in lung adenocarcinoma cells. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
Entities: CellLine
Chemical
Disease
Gene
Species
Keywords:
Cisplatin; PD-L1; anti-tumor; ginsenoside Rh2; lung adenocarcinoma; superoxide.
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Year: 2020
PMID: 31814556 DOI: 10.2174/1871520619666191209091230
Source DB: PubMed Journal: Anticancer Agents Med Chem ISSN: 1871-5206 Impact factor: 2.505