ArticleThe Journal of biological chemistry2012
Cyclin-dependent kinase-1 (Cdk1)/cyclin B1 dictates cell fate after mitotic arrest via phosphoregulation of antiapoptotic Bcl-2 proteins.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 60 citations in OpenAlex.
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- BAD sensitizes breast cancer cells to docetaxel with increased mitotic arrest and necroptosis.Scientific reports · 2020Article
- Identifying fates of cancer cells exposed to mitotic inhibitors by quantitative phase imaging.The Analyst · 2019Article
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- The impact of phosphatases on proliferative and survival signaling in cancer.Cellular and molecular life sciences : CMLS · 2018Review
- Perturbing mitosis for anti-cancer therapy: is cell death the only answer?EMBO reports · 2018Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The prevailing model suggests that cell fate after mitotic arrest depends on two independent and competing networks that control cyclin B1 degradation and the generation of death signals. However, recent evidence for Cdk1/cyclin B1-mediated phosphorylation and inactivation of antiapoptotic Bcl-2 proteins suggests the existence of significant cross-talk and interdependence between these pathways. Further, the nature of the mitotic death signals has remained elusive. In this study, we sought to test the hypothesis that fate after mitotic arrest is dictated by the robustness of Cdk1/cyclin B1 signaling to Bcl-2 proteins and to identify signals that may represent a mitotic death signature. We show that when treated with Taxol, slippage-resistant HT29 colon carcinoma cells display robust Cdk1 activity and extensive Mcl-1/Bcl-x(L) phosphorylation and die in mitosis, whereas slippage-prone DLD-1 colon carcinoma cells display weak Cdk1 activity and partial and transient Mcl-1/Bcl-x(L) phosphorylation and die in subsequent interphase or survive. Furthermore, modulation of this signaling axis, either by inhibition of Cdk1 in slippage-resistant HT29 or by enforcing mitotic arrest in slippage-prone DLD-1 cells, evokes a switch in fate, indicating that the strength of Cdk1 signaling to Bcl-2 proteins is a key determinant of outcome. These findings provide novel insight into the pathways that regulate mitotic death, suggest that the robustness of these signaling events may be useful as a marker to define susceptibility to antimitotic drugs, and encourage a revision in the current model describing fate after mitotic arrest.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.