Sodium selenite induces apoptosis in colon cancer cells via Bax-dependent mitochondrial pathway

Abstract

OBJECTIVES: We aimed to elucidate a possible mechanism of action by investigating the effects of selenium (Se) on cell cycle arrest and apoptosis in colorectal cancer cells (HCT116 cells and SW620 cells). Materials and methods: The colorectal cancer cells were treated with varying concentrations of Se (1 microM, 5 microM and 10 microM) for 24 hours. The effects of Se on cell cycle, apoptosis, mitochondrial transmembrane potential and apoptosis related proteins were examined by flow cytometry assessment and immunoblotting. Results: Se induced G2/M cell cycle arrest and apoptosis in colorectal cancer cells (HCT116 cells and SW620 cells) in a dose-dependent manner. Bax (Bcl2 associated X protein) was up-regulated and Bcl-2 (B cell linphoma gene-2) was down-regulated after Se treatment in both cells in a dose-dependent manner. Se caused increased loss of MMP (matrix metalloproteinase) and induced Bax translocation from cytosol into mitochondria and caspase 3 activation in both colorectal cancer cells in a dose-dependent manner. Conclusions: Se induced G2/M cell cycle arrest and apoptosis in both colorectal cancer cells via Bax-dependent mitochondrial pathway.