Journal
CURRENT OPINION IN GENETICS & DEVELOPMENT
Volume 21, Issue 1, Pages 12-20Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.gde.2010.12.001
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Funding
- NIAID NIH HHS [R01 AI044828-13, R01 AI044828, R01 AI040646, R01 AI047891-13, R01 AI047891, R01 AI040646-16] Funding Source: Medline
- NIGMS NIH HHS [R01 GM096208, R37 GM052735-21, R37 GM052735, R01 GM096208-01] Funding Source: Medline
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The mitochondrial pathway of apoptosis constitutes one of the main safeguards against tumorigenesis. The BCL-2 family includes the central players of this pathway that regulate cell fate through the control of mitochondrial outer membrane permeabilization (MOMP), and important progress has been made in understanding the dynamic interactions between proapoptotic and anti-apoptotic BCL-2 proteins. In particular, recent studies have delineated a stepwise model for the induction of MOMP. BCL-2 proteins are often dysregulated in cancer, leading to increased survival of abnormal cells; however, recent studies have paradoxically shown that apoptosis induction can under some circumstances drive tumor formation, perhaps by inducing compensatory proliferation under conditions of cellular stress. These observations underline the complexity of BCL-2 protein function in oncogenesis.
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