sulphoraphene and Colonic-Neoplasms

Cruciferous vegetables harbor a number of isothiocyanates that have been recognized for their cancer-related properties. Out of these, sulforaphene (a naturally occurring derivative of sulforaphane) has received little attention in studies of colon cancer and its mechanism of action remains to be elucidated.. We observed that sulforaphene inhibited growth of human colon cancer cell lines HCT116, HT-29, KM12, SNU-1040, and DLD-1, while exhibiting negligible toxicity toward nonmalignant cells. Sulforaphene induced G2/M phase cell cycle arrest and apoptosis of colon cancer cells analyzed by flow cytometry, concomitant with phosphorylation of CDK1 and CDC25B at inhibitory sites, and upregulation of the p38 and JNK pathways. It was further determined that sulforaphene is a potent inhibitor of microtubule polymerization while generating reactive oxygen species via the depletion of glutathione. These observations further extended into inhibitory effects against colon tumor growth in a mouse xenograft model.. These findings demonstrate that sulforaphene may contribute to the anti-tumor effects of cruciferous vegetables that contain sulforaphene and other isothiocyanates.

Topics: Animals; Antineoplastic Agents; Apoptosis; CDC2 Protein Kinase; cdc25 Phosphatases; Cell Line, Tumor; Cell Survival; Colonic Neoplasms; G2 Phase Cell Cycle Checkpoints; Glutathione; HCT116 Cells; HT29 Cells; Humans; Isothiocyanates; M Phase Cell Cycle Checkpoints; Male; MAP Kinase Signaling System; Mice; Mice, Nude; Microtubules; p38 Mitogen-Activated Protein Kinases; Reactive Oxygen Species; Xenograft Model Antitumor Assays