Regulation of cancer cell survival by BCL2 family members upon prolonged mitotic arrest: opportunities for anticancer therapy.
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.
Team Cell Survival and Tumor Escape in Breast Cancer, UMR 892 INSERM /6299 CNRS, University of Nantes, Nantes, France. sophie.barille@inserm.fr
Sophie
S
Barillé-Nion
Nourdine
N
Bah
Eloïse
E
Véquaud
Philippe
P
Juin
D000818:Animals; D050256:Antimitotic Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D059447:Cell Cycle Checkpoints / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects*; D006801:Humans; D051379:Mice; D008938:Mitosis / Q000187:drug effects*; D009369:Neoplasms / Q000188:drug therapy*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000037:antagonists & inhibitors*
D050256:Antimitotic Agents; D019253:Proto-Oncogene Proteins c-bcl-2