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The regulation of mitochondrial metabolism by the Bcl-2 family of pro-survival proteins: new therapeutic opportunities for targeting cancer cells

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journal contribution
posted on 2013-01-01, 00:00 authored by Mark GuthridgeMark Guthridge, Melissa Brown, Andrew Wei
Since the identification of the first tumor oncogenesin the 1970s, advances in our understanding of the molecular basis for cellular transformation have continued at a breathtaking rate. Yet compared to other classical hallmarks of cancer such as evading apoptosis, self-sufficiency in growth signals, insensitivity to anti-growth signals and limitless replicative potential, the mechanisms by which transformed cells undergo metabolic reprogramming leading to rampant glycolysis (termed the “Warburg effect”) remain poorly defined. Several very recent studies have revealed that, in addition to their well-established roles in regulating intrinsic apoptosis programs, the Bcl-2 family of pro-survival proteins are also important regulators of mitochondrial respiration and energy generation in cancers such as Acute Myeloid Leukemia (AML). This article discusses some recent advances in our understanding of how the Bcl-2 family of proteins regulate cellular metabolism and how exploiting metabolic vulnerabilities in transformed cells by direct targeting of the Bcl-2 proteins may provide new clinical avenues for the treatment of cancer.

History

Journal

Journal of hematology & thromboembolic diseases

Volume

1

Article number

1000121

Location

Hyderabad, India

ISSN

2329-8790

Language

eng

Publication classification

C1.1 Refereed article in a scholarly journal

Copyright notice

2013, Wei AH, et al.

Issue

4

Publisher

Longdom Group

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