Title:Ginsenoside Rh2 Improves the Cisplatin Anti-tumor Effect in Lung Adenocarcinoma A549 Cells via Superoxide and PD-L1
VOLUME: 20 ISSUE: 4
Author(s):Yingying Chen, Yuqiang Zhang, Wei Song, Ying Zhang, Xiu Dong and Mingqi Tan*
Affiliation:Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, 110042, Liaoning Province, Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, 110042, Liaoning Province, Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, 110042, Liaoning Province, Oncology Medicine Department, Shengjing Hospital of China Medical University, Shenyang, 110042, Liaoning Province, School of Preclinical Medicine, Liaoning University of Traditional Chinese Medicine, 79 Chong Shan Dong Lu, Huanggu District, Shenyang, Liaoning, 110847, Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, 110042, Liaoning Province
Keywords:Cisplatin, ginsenoside Rh2, lung adenocarcinoma, PD-L1, superoxide, anti-tumor.
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.