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    DNA damage-induced cell death is enhanced by progression through mitosis

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    Authors
    Varmark, Hanne
    Sparks, Cynthia A.
    Nordberg, Joshua J.
    Koppetsch, Birgit S.
    Theurkauf, William E.
    UMass Chan Affiliations
    Department of Cell Biology
    Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2009-08-29
    Keywords
    Caspases
    Cell Death
    Cell Line
    Cell Line, Tumor
    Cytokinesis
    *DNA Damage
    Embryonic Stem Cells
    HCT116 Cells
    Humans
    Kinetics
    *Mitosis
    Tumor Suppressor Protein p53
    Life Sciences
    Medicine and Health Sciences
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2897049/
    Abstract
    Progression through the G(2)/M transition following DNA damage is linked to cytokinesis failure and mitotic death. In four different transformed cell lines and two human embryonic stem cell lines, we find that DNA damage triggers mitotic chromatin decondensation and global phosphorylation of histone H2AX, which has been associated with apoptosis. However, extended time-lapse studies in HCT116 colorectal cancer cells indicate that death does not take place during mitosis, but 72% of cells die within 3 days of mitotic exit. By contrast, only 11% of cells in the same cultures that remained in interphase died, suggesting that progression through mitosis enhances cell death following DNA damage. These time-lapse studies also confirmed that DNA damage leads to high rates of cytokinesis failure, but showed that cells that completed cytokinesis following damage died at higher rates than cells that failed to complete division. Therefore, post-mitotic cell death is not a response to cytokinesis failure or polyploidy. We also show that post-mitotic cell death is largely independent of p53 and is only partially suppressed by the apical caspase inhibitor Z-VAD-FMK. These findings suggest that progression through mitosis following DNA damage initiates a p53- and caspase-independent cell death response that prevents propagation of genetic lesions.
    Source

    Cell Cycle. 2009 Sep 15;8(18):2951-63. Epub 2009 Sep 16.

    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/39312
    PubMed ID
    19713770
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