RESUMO
Transforming growth factorß1 (TGFß1) has been demonstrated to promote epithelialmesenchymal transition (EMT), invasion and proliferation in tumors via the activation of Rac1 and ßcatenin signaling pathways. The present study investigated the effects of diallyl disulfide (DADS) on TGFß1induced EMT, invasion and growth of gastric cancer cells. TGFß1 treatment augmented EMT and invasion, concomitantly with increased expression of TGFß1, Rac1 and ßcatenin in gastric cancer cells. DADS downregulated the expression levels of TGFß1, Rac1 and ßcatenin. DADS, TGFß1 receptor inhibitor as well as Rac1 inhibitor antagonized the upregulation of the TGFß1induced expression of these genes, abolishing the enhanced effects of TGFß1 on EMT and invasion. Blocking the TGFß1 receptor through inhibition resulted in the decreased expression of Rac1 and ßcatenin. Rac1 inhibitor reduced the TGFß1induced ßcatenin expression. In addition, DADS and the aforementioned inhibitors attenuated the TGFß1induced tumor growth and the expression changes of Ecadherin, vimentin, Ki67 and CD34 in nude mice. These data indicated that the blockage of TGFß1/Rac1 signaling by DADS may be responsible for the suppression of EMT, invasion and tumor growth in gastric cancer.