BCL-2 Emerges as an Attractive Target in Solid and Hematologic Cancers

Erin Burns, PhD
Published: Tuesday, Mar 05, 2019
The gene encoding B-cell lymphoma-2 (BCL-2) was identified more than 30 years ago in a patient with follicular lymphoma (FL) who had a chromosomal translocation that led to dysregulated BCL-2 expression.1 When the BCL-2 gene product was reported to block cell death instead of enhancing cell proliferation, which was the expected action of oncogenes, the link among BCL-2, apoptosis, and cancer was established.2,3 This finding led to the idea that impaired apoptosis was an important feature required for tumorigenesis.4

It is unclear at this time whether these concerns will remain in clinical trials; however, promising study results support the potential of BH3 mimetics to dramatically improve survival in patients with various cancer types.

Role of BCL-2 in Cancer

The BCL-2 family proteins are important for regulation of cell death at both the mitochondria and the endoplasmic reticulum. The proteins function to regulate mitochondrial outer membrane permeabilization through a coordinated series of protein–protein and protein–membrane interactions that are associated with protein conformational changes that control pore formation in organelle membranes.10,11 When BCL-2 is overexpressed, it blocks BAX, an apoptotic protein, and prevents mitochondrial pore formation and inhibits the release of cytochrome C, which leads to inhibited or reduced cell death.12
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