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

Abstract

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.

Keywords: NF-κB; PI3K/Akt; astragaloside IV; epithelial-mesenchymal transition; gastric cancer.