Bax Protein in Cancer Treatment

Jin-Hyuk Choi

doi:10.5124/jkma.2007.50.11.1016

J Korean Med Assoc > Volume 50(11); 2007 > Article

Choi: Bax Protein in Cancer Treatment

Continuing Education Column

Journal of the Korean Medical Association

Journal of the Korean Medical Association 2007; 50(11): 1016-1022.

Published online: November 30, 2007

DOI: http://dx.doi.org/10.5124/jkma.2007.50.11.1016

Bax Protein in Cancer Treatment

Jin-Hyuk Choi, MD

Department of Hematology-Oncology, Ajou University College of Medicine, Korea. jhchoimd@ajou.ac.kr

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.

Apoptosis; Bax protein; Low expression; Resistance; Prognostic factor

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Figure 1

Apoptosis signaling pathways.