“Prognostic Significance of Bax and Bcl-2 Gene Expression and Their Ratio in Carcinogenesis”

Gehan Abdel Naser Abdel Rahman

Department of Oral and Maxillofacial Pathology department, Faculty of Oral and Dental Medicine, South Valley University, Qena 83523 & Department of Oral Pathology, Faculty of Dentistry, Minia University, Minia 61519, Egypt

Dr. Gehan Abdel Naser Abdel Rahman, Department of Oral and Maxillofacial Pathology department, Faculty of Oral and Dental Medicine, South Valley University, Qena 83523, Egypt.

Keywords: Bax; Apoptosis; Bcl-2; Mitochondrial Membrane; Intrinsic Apoptotic Pathway

Abstract

The ability of malignant cells to escape from apoptosis is a hallmark of cancer; cancer cells show several characteristics that would readily stimulate apoptosis in normal cells-such as, they violate checkpoints of cell cycle as well as withstanding the exposure to cytotoxic agents; Because of these characteristics, cancer cells tend to survive. Apoptosis is an effective barrier to developing cancer; avoiding apoptosis is important to development of tumor and resistance to cancer therapy. Members of bcl-2 family regarded as important mediators of apoptosis in health and disease, often shown to be deregulated in tumor and lead to the survival of malignant clones. Bax and Bcl-2 are the main members of bcl-2 family that have critical role in cancer progression and inhibition of intrinsic apoptotic pathway stimulated by mitochondrial dysfunction. The balance of pro- (Bax) and anti-apoptotic (Bcl-2) genes can determine the fate of malignant cell. Bcl-2 protein family is the hallmark of apoptosis regulation and disturbance of apoptosis signaling pathways plays critical role in carcinogenesis. Members of Bcl-2 genes were found to be differentially expressed in many types of malignancies. The Bcl-2 protein family is possibly correlated to cancer pathophysiology and resistance to conventional chemotherapy, through its role in regulation of apoptosis. The aim of study was to explain the role of Bax/Bcl-2 Ratio in tumor progression and the effect of its disturbance in carcinogenesis.

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