Bax is essential for death receptor-mediated apoptosis in human colon cancer cells.

To demonstrate the role of Bax in death receptor-induced apoptosis in the human colon cancer HCT116 cells. We treated HCT116 cells and HCT116 with p53(-/-) (KO) by 0.1 mu g/mL TRAIL for 24 hours, which indicated that HCT116 parental cells are sensitive to p53-independent death receptor-induced apoptosis. Although the p53 signaling pathway is totally intact in this system, the down-regulation of Bax in HCT116 cells is dramatically resistant to TRAIL and failed to undergo apoptosis. However, the over-expression of Bax can rescue the sensitivity of apoptosis induced by the death receptor. Our study has revealed an essential role for Bax in death receptor-induced apoptosis in the human colon cancer HCT116 cells. It may aid in a molecular understanding of possible defects in signal transduction and a regulation of the death receptor-induced apoptotic process.