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

Abstract

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 beta 1 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 beta 1 expression and the roles of talin and rab25 in integrin beta 1 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 beta 1 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 beta 1 expression even in the absence of rab25. Confocal microscopy revealed a dose-dependent increase in integrin beta 1 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 beta 1 expression through a talin-mediated pathway rather than through rab25.