Department of Ultrasound, Huaihe Hospital of Henan University, Kaifeng, 475000, Henan, China.
Phytother Res. 2018 Jul;32(7):1289-1296. doi: 10.1002/ptr.6057. Epub 2018 Feb 26.
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.
黄芪甲苷（AS-IV）已被报道具有抑制癌细胞转移的活性。然而，尚不清楚 AS-IV 是否能抑制上皮间质转化（EMT），即促进转移的细胞去分化程序。本研究旨在研究 AS-IV 对胃癌（GC）细胞 EMT 的作用及其机制。结果表明，AS-IV 显著抑制 GC 细胞的活力、侵袭和迁移。转化生长因子β1（TGF-β1）诱导 E-钙黏蛋白向 N-钙黏蛋白的转换以及波形蛋白和转移相关基因的表达，而 AS-IV 则逆转了这种诱导。此外，AS-IV 抑制了 TGF-β1 诱导的 PI3K/Akt/NF-κB 激活。抑制 PI3K/Akt/NF-κB 通路逆转了 TGF-β1 诱导的 EMT。总之，AS-IV 通过抑制 GC 细胞中的 PI3K/Akt/NF-κB 通路抑制 TGF-β1 诱导的 EMT。AS-IV 可能是治疗 GC 的有效候选药物。
