Affiliation:
1. Department of Pathology, Taizhou People’s Hospital Affiliated to Nanjing University of Chinese Medicine, Taizhou, Jiangsu, China
2. Institute of Clinical Medicine, Taizhou People’s Hospital Affiliated to Nanjing University of Chinese Medicine, Taizhou, Jiangsu, China
Abstract
Ginsenoside 20(S)-Rg3 is identified as an active saponin monomer which derived from red ginseng and is demonstrated to play an anti-tumor role in diverse cancers. MicroRNAs (miRNAs) are important regulators in the progression of cancers, containing esophageal squamous cell carcinoma (ESCC). It was reported that microRNA 324-5p (miR-324-5p) exerted critical functions in some cancers; however, the detailed molecular mechanism of miR-324-5p mediated by 20(S)-Rg3 to suppress cell viability in ESCC has not been explored. Herein, we explored the function of 20(S)-Rg3 or miR-324-5p on ESCC cell viability by MTT assay, colony formation assay, flow cytometry analysis and western blot analysis. The binding of miR-324-5p to its target gene, proteasome activator subunit 3 (PSME3), was confirmed through RNA pull down and luciferase reporter assays. The results indicated that 20(S)-Rg3 significantly inhibited cell viability and the cell cycle and facilitated cell apoptosis. Furthermore, this effect was strengthened with the increased concentration of 20(S)-Rg3. Moreover, we found that miR-324-5p level was increased under 20(S)-Rg3 treatment. Additionally, overexpressed miR-324-5p inhibited ESCC cell viability, and downregulated miR-324-5p recovered inhibited cell viability caused by 20(S)-Rg3. Further exploration verified that miR-324-5p targeted PSME3, and PSME3 deficiency countervailed the effect of miR-324-5p inhibition on ESCC cell viability under 20(S)-Rg3 treatment. Conclusively, 20(S)-Rg3 suppresses cell viability in ESCC via mediating miR-324-5p-targeted PSME3.
Funder
Taizhou Society Development Project, Jiangsu, China
Subject
Health, Toxicology and Mutagenesis,Toxicology,General Medicine
Cited by
8 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献