Ginsenoside CK Inhibits TGF-β-Induced Epithelial-Mesenchymal Transition in A549 Cell via SIRT1

• Published in: BioMed research international Vol. 2021; pp. 9140191 - 11
• Main Authors: Sun, Mingyang, Zhuang, Xuefeng, Lv, Guangfu, Lin, Zhe, Huang, Xiaowei, Zhao, Jiarui, Lin, He, Wang, Yuchen
• Format: Journal Article
• Language: English
• Published: United States Hindawi 2021; Hindawi Limited
• Subjects: A549 Cells; Animals; Antibodies; Biotechnology; Cadherins - metabolism; Cell culture; Cell Line, Tumor; Cell Movement - drug effects; Down-Regulation - drug effects; E-cadherin; Epithelial-Mesenchymal Transition - drug effects; Experiments; Ginsenosides; Ginsenosides - pharmacology; Homology; Humans; Laboratory animals; Lung cancer; Lung Neoplasms - metabolism; Male; Medical prognosis; Mesenchyme; Metabolites; Metastases; Metastasis; Mice; Mice, Inbred BALB C; Mice, Nude; Molecular modelling; Non-small cell lung carcinoma; Proteins; Saponins; SIRT1 protein; Sirtuin 1 - metabolism; Small cell lung carcinoma; Software; Transforming Growth Factor beta - metabolism; Transforming growth factor-b; Tumors; Up-Regulation - drug effects; Vimentin; Vimentin - metabolism; Beijing China; United Kingdom > UK; United States > US; China
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2021/9140191

Ginsenoside CK is the main metabolite of protopanaxadiol saponins in intestinal bacteria. Previous studies have shown that ginsenoside CK can affect many aspects of tumor development through a variety of mechanisms. However, few studies have reported the antimetastatic effects of ginsenoside CK in non-small-cell lung cancer (NSCLC). In this study, we explored the effect of ginsenoside CK on epithelial-mesenchymal transition (EMT) induced by TGF-β in A549 cells and the potential molecular mechanisms. Our data showed that ginsenoside CK effectively prevented TGF-β-induced EMT, as indicated by the upregulation of E-cadherin and downregulation of vimentin. Furthermore, ginsenoside CK inhibited the metastatic ability of A549 cells in the tail vein lung metastasis model of nude mice. Additionally, ginsenoside CK decreased the expression of silent information regulator 2 homolog 1 (SIRT1) in the inhibition of EMT induced by TGF-β. Moreover, the antimetastatic effect of ginsenoside CK was reversed by SIRT1 overexpression. Generally, our results indicated the antimetastatic effect and underlying mechanism of ginsenoside CK on TGF-β-induced EMT in A549 cells, suggesting that ginsenoside CK can be used as an effective antineoplastic agent.