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.
Highlights
According to statistics, lung cancer was one of the top three cancers worldwide in 2018 [1]
We investigated the mRNA levels of epithelial-mesenchymal transition (EMT)-related transcription factors Snail, Slug, and Zeb1 to evaluate the anti-EMT effects of ginsenoside CK
These data indicate that ginsenoside CK treatment inhibited Transforming growth factor-β (TGF-β)-induced EMT in A549 cells
Summary
Lung cancer was one of the top three cancers worldwide in 2018 [1]. Among all types of lung cancer, non-small-cell lung cancer (NSCLC) accounts for more than 85% of all lung cancer patients. Clinical data showed that approximately 90% of lung cancer patients die due to tumor metastasis [4, 5]. Transforming growth factor-β (TGF-β) is an important growth inhibitor that can inhibit the growth of most normal cells; it plays an important role in regulating various cell behaviors, including invasion, migration, differentiation, and changes in the microenvironment [6]. TGF-β1 promotes tumor migration and invasion and inhibits tumor cell growth [6, 7]. Overexpression of TGF-β1 in advanced stages of lung cancer can promote tumor growth and metastasis [8]. For patients with NSCLC, high TGF-β1 expression is an important prognostic parameter after operative treatment
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