Does met inactivation by S-allylcysteine suppress the migration and invasion of nasopharyngeal cancer cells induced by hepatocyte growth factor?
These results suggest that SAC inhibited not only Met activation but also the downstream FAK, Slug, and MMP expression. Finally, SAC may be a potent anticancer compound for nasopharyngeal cancer treated with radiotherapy.
This study is the first to report that the ERalpha mediates susceptibility to early atherosclerosis in male mice by a testosterone-dependent pathway, suggesting that local production of estrogen from testosterone in the vessel wall may promote atheroma formation in ERalpha males. Our findings may have implications for selective targeting of ERalpha in atherosclerotic disease.