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    Inhibition of Bcl-xL sensitizes cells to mitotic blockers, but not mitotic drivers.

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    Authors
    Bennett, A
    Sloss, O
    Topham, C
    Nelson, L
    Tighe, A
    Taylor, Stephen S
    Affiliation
    Manchester Cancer Research Centre, University of Manchester, Wilmslow Road, Manchester M20 4QL
    Issue Date
    2016-08
    
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    Abstract
    Cell fate in response to an aberrant mitosis is governed by two competing networks: the spindle assembly checkpoint (SAC) and the intrinsic apoptosis pathway. The mechanistic interplay between these two networks is obscured by functional redundancy and the ability of cells to die either in mitosis or in the subsequent interphase. By coupling time-lapse microscopy with selective pharmacological agents, we systematically probe pro-survival Bcl-xL in response to various mitotic perturbations. Concentration matrices show that BH3-mimetic-mediated inhibition of Bcl-xL synergises with perturbations that induce an SAC-mediated mitotic block, including drugs that dampen microtubule dynamics, and inhibitors targeting kinesins and kinases required for spindle assembly. By contrast, Bcl-xL inhibition does not synergize with drugs which drive cells through an aberrant mitosis by overriding the SAC. This differential effect, which is explained by compensatory Mcl-1 function, provides opportunities for patient stratification and combination treatments in the context of cancer chemotherapy.
    Citation
    Inhibition of Bcl-xL sensitizes cells to mitotic blockers, but not mitotic drivers. 2016, 6 (8): Open Biol
    Journal
    Open Biology
    URI
    http://hdl.handle.net/10541/619909
    DOI
    10.1098/rsob.160134
    PubMed ID
    27512141
    Type
    Article
    Language
    en
    ISSN
    2046-2441
    ae974a485f413a2113503eed53cd6c53
    10.1098/rsob.160134
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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