Diallyl disulfide inhibits TGF‑β1‑induced upregulation of Rac1 and β‑catenin in epithelial‑mesenchymal transition and tumor growth of gastric cancer.

Transforming growth factor‑β1 (TGF‑β1) has been demonstrated to promote epithelial‑mesenchymal transition (EMT), invasion and proliferation in tumors via the activation of Rac1 and β‑catenin signaling pathways. The present study investigated the effects of diallyl disulfide (DADS) on TGF‑β1‑induced EMT, invasion and growth of gastric cancer cells. TGF‑β1 treatment augmented EMT and invasion, concomitantly with increased expression of TGF‑β1, Rac1 and β‑catenin in gastric cancer cells. DADS downregulated the expression levels of TGF‑β1, Rac1 and β‑catenin. DADS, TGF‑β1 receptor inhibitor as well as Rac1 inhibitor antagonized the upregulation of the TGF‑β1‑induced expression of these genes, abolishing the enhanced effects of TGF‑β1 on EMT and invasion. Blocking the TGF‑β1 receptor through inhibition resulted in the decreased expression of Rac1 and β‑catenin. Rac1 inhibitor reduced the TGF‑β1‑induced β‑catenin expression. In addition, DADS and the aforementioned inhibitors attenuated the TGF‑β1‑induced tumor growth and the expression changes of E‑cadherin, vimentin, Ki‑67 and CD34 in nude mice. These data indicated that the blockage of TGF‑β1/Rac1 signaling by DADS may be responsible for the suppression of EMT, invasion and tumor growth in gastric cancer.