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Ginsenoside CK Inhibits TGF-β-Induced Epithelial-Mesenchymal Transition in A549 Cell via SIRT1
Mingyang Sun1, Xuefeng Zhuang1, Guangfu Lv1
1Department of Pharmacology, School of Pharmaceutical Sciences, Changchun University of Chinese Medicine, Changchun, Jilin 130117, China.
Abstract:
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.
Insights
Ginsenoside CK, a metabolite from intestinal bacteria, effectively inhibits non-small-cell lung cancer (NSCLC) metastasis by preventing epithelial-mesenchymal transition (EMT) and targeting SIRT1. This suggests its potential as an antineoplastic agent.
Area of Science:
- Pharmacology and Oncology
- Molecular Biology
- Cancer Metastasis Research
Background:
- Ginsenoside CK is a key metabolite of protopanaxadiol saponins.
- Ginsenoside CK is known to influence tumor development via multiple mechanisms.
- Limited research exists on the antimetastatic effects of ginsenoside CK in non-small-cell lung cancer (NSCLC).
Purpose of the Study:
- To investigate the antimetastatic effects of ginsenoside CK on non-small-cell lung cancer (NSCLC).
- To explore the molecular mechanisms underlying ginsenoside CK's action on epithelial-mesenchymal transition (EMT) induced by TGF-β in A549 cells.
Main Methods:
- Utilized A549 cells to study TGF-β-induced epithelial-mesenchymal transition (EMT).
- Assessed changes in E-cadherin and vimentin expression.
- Employed a tail vein lung metastasis model in nude mice.
- Investigated the role of silent information regulator 2 homolog 1 (SIRT1) and its modulation by ginsenoside CK.
Main Results:
- Ginsenoside CK effectively inhibited TGF-β-induced EMT, upregulating E-cadherin and downregulating vimentin.
- Ginsenoside CK demonstrated inhibition of metastatic potential in A549 cells within a lung metastasis model.
- Ginsenoside CK reduced silent information regulator 2 homolog 1 (SIRT1) expression during TGF-β-induced EMT.
- Overexpression of SIRT1 reversed the antimetastatic effects of ginsenoside CK.
Conclusions:
- Ginsenoside CK exhibits significant antimetastatic effects in non-small-cell lung cancer (NSCLC) models.
- The mechanism involves the inhibition of TGF-β-induced epithelial-mesenchymal transition (EMT) potentially through modulation of SIRT1.
- Ginsenoside CK shows promise as a potential antineoplastic agent for treating NSCLC.
