S-Allylmercaptocysteine induces G2/M phase arrest and apoptosis via ROS-mediated p38 and JNK signaling pathway in human colon cancer cells in vitro and in vivo

Abstract

S-Allylmercaptocysteine (SAMC), a water-soluble organosulfur garlic derivative, has exhibited potential antitumor activity in various malignancies. Here we explored the effects of SAMC on colon cancer in vitro and in vivo and further elucidated the underlying molecule mechanisms. In this study, we found that SAMC potently suppressed cell viability and induced G2/M phase arrest and apoptosis in colon cancer HCT116 cells. Further studies showed that reactive oxygen species (ROS) attributed to SAMC-induced cell cycle arrest and apoptosis, which was attenuated by N-acetyl cysteine (NAC), an ROS scavenger. Moreover, we found that SAMC activated p38 and c-Jun N-terminal kinase (JNK) signal pathway, which was also blocked by NAC. Finally, SAMC administration in mice effectively delayed the growth of HCT116 xenografts without signs of toxicity. In conclusion, SAMC induced cell cycle G2/M phase arrest and apoptosis via ROS-mediated p38 and JNK signaling pathway in colon cancer HCT116 cells. In light of these results, SAMC may be a promising agent for anticancer therapy against colon cancer.