Cancer-specific cytotoxicity of curcumin through regulation of integrin β1 expression in colon cancer.

Curcumin has attracted attention for its nontoxic chemopreventive effects; however, the pathways underlying these effects in colon cancer remain unclear. We investigated the potential interplay between curcumin and integrin β1 in colon cancer. Human colon cancer (HCT) 116 cell line and fibroblast cells were treated with curcumin, and cell proliferation was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and western blotting. Using western blotting and confocal microscopy in curcumin-treated HCT116 cells, we analyzed integrin β1 expression and the roles of talin and rab25 in integrin β1 activation by curcumin. Curcumin significantly decreased the survival of HCT116 cells but did not significantly affect the survival of fibroblast cells. Moreover, curcumin significantly increased integrin β1 expression in HCT116 cells, which was primarily mediated by talin. In contrast, rab25 expression remained unchanged after curcumin treatment. Using rab25-specific small interfering ribonucleic acid knock-down experiments, we confirmed that curcumin increased integrin β1 expression even in the absence of rab25. Confocal microscopy revealed a dose-dependent increase in integrin β1 and talin expression, with consistent spatial distribution patterns in response to curcumin. This study reports that curcumin acts as an anticancer agent in colon cancer by modulating integrin β1 expression through a talin-mediated pathway rather than through rab25.