Bax Protein in Cancer Treatment.
10.5124/jkma.2007.50.11.1016
- Author:
Jin Hyuk CHOI
1
Author Information
1. Department of Hematology-Oncology, Ajou University College of Medicine, Korea. jhchoimd@ajou.ac.kr
- Publication Type:Original Article
- Keywords:
Apoptosis;
Bax protein;
Low expression;
Resistance;
Prognostic factor
- MeSH:
Apoptosis;
bcl-2-Associated X Protein*;
Biopsy;
Breast;
Cell Death;
Drug Therapy;
Head and Neck Neoplasms;
Humans;
Permeability;
Radiotherapy
- From:Journal of the Korean Medical Association
2007;50(11):1016-1022
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Apoptosis is the major mechanism of cancer cell death by chemotherapy as well as radiation. Bax is a critical downstream mediator of apoptosis which belonged to the Bcl-2 family, and it initiates a mitochondrial permeability shift transition, leading to the activation of downstream apoptosis signaling pathways. Bax protein is activated by BH3-only proteins or p53, while prosurvival Bcl-2 family proteins suppress the function of Bax protein. Therefore, genetic defects in Bax may not only result in intrinsic biologic aggressiveness but also cause resistance to the cytotoxic effects of chemotherapy and radiotherapy. The role of low expression of Bax protein as a poor prognostic or predictive factor has been reported in several malignancies such as breast, colorectal, ovarian, esophageal, and head and neck cancer. Various novel therapeutic approaches targeting Bax protein are under investigation. In addition, several studies suggest that the evaluation of Bax protein with a pretreatment biopsy specimen may provide valuable information to the oncologist for the selection of appropriate therapeutic modality for the patients.
