Regulation of cancer cell survival by BCL2 family members upon prolonged mitotic arrest: opportunities for anticancer therapy.

Abstract

Attacking cancer cell survival defense by targeting B-Cell Lymphoma 2 (BCL2) family of anti-apoptotic proteins may provide a powerful means to improve chemotherapy efficiency. This could be particularly relevant to anti-mitotic-based therapy, where tumor response relates to a competing network between mitotic cell death signaling and mitotic slippage as an adaptative response to a leaky mitotic checkpoint. In this review, we focus on recent findings that point out the major role played by BCL2 family members in response to anti-mitotic agents, which reveal dependence of cancer cell survival on BCL2 homologs during mitotic arrest and after mitotic slippage. Finally, we discuss pre-clinical data combining anti-mitotic agents with BCL2 inhibitors.

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@article{BarillNion2012RegulationOC, title={Regulation of cancer cell survival by BCL2 family members upon prolonged mitotic arrest: opportunities for anticancer therapy.}, author={Sophie Barill{\'e}-Nion and Nourdine Bah and Elo{\"{i}se V{\'e}quaud and Philippe Paul Juin}, journal={Anticancer research}, year={2012}, volume={32 10}, pages={4225-33} }