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Astragaloside IV inhibits TGF‐β1‐induced epithelial‐mesenchymal transition through inhibition of the PI3K/Akt/NF‐κB pathway in gastric cancer cells

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 β1 (TGF‐β1), whereas AS‐IV reversed the induction. In addition, AS‐IV inhibited TGF‐β1‐induced activation of PI3K/Akt/NF‐κB. Inhibition of the PI3K/Akt/NF‐κB pathway reversed TGF‐β1‐induced EMT. In conclusion, AS‐IV inhibited TGF‐β1‐induced EMT through inhibition of the PI3K/Akt/NF‐κB pathway in GC cells. AS‐IV might be an effective candidate for the treatment for GC.