Astragaloside IV suppresses transforming growth factor-β1-induced epithelial-mesenchymal transition through inhibition of Wnt/β-catenin pathway in glioma U251 cells

Astragaloside IV (AS#IV) has previously demonstrated antitumoractivity. We investigated the effect and mechanisms of AS#IV in relation to epithelial-mesenchymal transition (EMT), viainterference with the Wnt/β-catenin signaling pathway in gliomaU251 cells. Induction of glioma U251 cells by transform...

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Veröffentlicht in:Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2020-07, Vol.84 (7), p.1345-1352
Hauptverfasser: Han, Jinming, Shen, Xiaohan, Zhang, Yong, Wang, Suying, Zhou, Leijie
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Sprache:eng
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Zusammenfassung:Astragaloside IV (AS#IV) has previously demonstrated antitumoractivity. We investigated the effect and mechanisms of AS#IV in relation to epithelial-mesenchymal transition (EMT), viainterference with the Wnt/β-catenin signaling pathway in gliomaU251 cells. Induction of glioma U251 cells by transforming growthfactor (TGF)#β1 activated EMT, including switching E#cadherin toN-cadherin and altering the expression of Wnt/β-catenin signalingpathway components such as vimentin, β-catenin, and cyclin-D1.AS-IV inhibited the viability, invasion, and migration of TGF-β1-induced glioma U251 cells. AS-IV also interfered with the TGF#β1-induced Wnt/β-catenin signaling pathway in glioma U251 cells.These findings indicate that AS#IV prohibits TGF#β1-induced EMTby disrupting the Wnt/β-catenin pathway in glioma U251 cells. AS#IV may thus be a potential candidate agent for treating glioma andother central nervous system tumors. Astragaloside IV interfered with the TGF-β1-induced Wnt/β-catenin signaling pathway in glioma cells.
ISSN:0916-8451
1347-6947
DOI:10.1080/09168451.2020.1737502