4.7 Article

Astragaloside IV inhibits TGF-1-induced epithelial-mesenchymal transition through inhibition of the PI3K/Akt/NF-B pathway in gastric cancer cells

Journal

PHYTOTHERAPY RESEARCH
Volume 32, Issue 7, Pages 1289-1296

Publisher

WILEY
DOI: 10.1002/ptr.6057

Keywords

astragaloside IV; epithelial-mesenchymal transition; gastric cancer; NF-B; PI3K; Akt

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Astragaloside IV (AS-IV) has been reported to possess anti-metastasis activity in cancer cells. However, it is unknown whether AS-IV could inhibit epithelial-mesenchymal transition (EMT), a cellular de-differentiation program that promotes metastasis, in cancer cells. The aim of this study was to study the effect and mechanism of AS-IV on EMT in gastric cancer (GC) cells. The results showed that AS-IV significantly inhibited cell viability, invasion, and migration of GC cells. The E-cadherin to N-cadherin switch and expression of Vimentin and metastasis-related genes were induced by transforming growth factor 1 (TGF-1), whereas AS-IV reversed the induction. In addition, AS-IV inhibited TGF-1-induced activation of PI3K/Akt/NF-B. Inhibition of the PI3K/Akt/NF-B pathway reversed TGF-1-induced EMT. In conclusion, AS-IV inhibited TGF-1-induced EMT through inhibition of the PI3K/Akt/NF-B pathway in GC cells. AS-IV might be an effective candidate for the treatment for GC.

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