Related Experiment Video
Updated: May 17, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles
Published on: October 5, 2012
Bax is essential for death receptor-mediated apoptosis in human colon cancer cells
Shunqin Zhu1, Tai Li, Juan Tan
1State Key Laboratory of Silkworm Genome Biology, Institute of Sericulture and Systems Biology, Southwest University, Chongqing, China.
Abstract:
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 μg/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.
More Related Videos
Related Concept Videos
The Intrinsic Apoptotic Pathway
The Extrinsic Apoptotic Pathway
Cellular Injury V: Apoptosis and Autophagy
Caspases
Apoptosis
Autophagic Cell Death
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...

