Ginsenoside CK Inhibits TGF-β-Induced Epithelial-Mesenchymal Transition in A549 Cell via SIRT1
| Autor: | Mingyang Sun, Xuefeng Zhuang, Guangfu Lv, Zhe Lin, Xiaowei Huang, Jiarui Zhao, He Lin, Yuchen Wang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
Mice Inbred BALB C Epithelial-Mesenchymal Transition Lung Neoplasms Article Subject General Immunology and Microbiology Ginsenosides Down-Regulation Mice Nude General Medicine Cadherins General Biochemistry Genetics and Molecular Biology Up-Regulation Mice Sirtuin 1 A549 Cells Cell Movement Transforming Growth Factor beta Cell Line Tumor Medicine Animals Humans Vimentin Research Article |
| Zdroj: | BioMed Research International BioMed Research International, Vol 2021 (2021) |
| ISSN: | 2314-6141 2314-6133 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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