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    Endopolyploidy in irradiated p53-deficient tumour cell lines: persistence of cell division activity in giant cells expressing Aurora-B kinase.

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    Authors
    Erenpreisa, Jekaterina
    Ivanov, Andrei
    Wheatley, Sally P
    Kosmacek, Elizabeth A
    Ianzini, Fiorenza
    Anisimov, Alim P
    Mackey, Mike
    Davis, Paul J
    Plakhins, Gregory
    Illidge, Timothy M
    Affiliation
    Latvia Biomedicine Research and Study Centre, Riga, Latvia. katrina@biomed.lu.lv
    Issue Date
    2008-09
    
    Metadata
    Show full item record
    Abstract
    Recent findings including computerised live imaging suggest that polyploidy cells transiently emerging after severe genotoxic stress (and named 'endopolyploid cells') may have a role in tumour regrowth after anti-cancer treatment. Until now, mostly the factors enabling metaphase were studied in them. Here we investigate the mitotic activities and the role of Aurora-B, in view of potential depolyploidisation of these cells, because Aurora-B kinase is responsible for coordination and completion of mitosis. We observed that endopolyploid giant cells are formed via different means in irradiated p53 tumours, by: (1) division/fusion of daughter cells creating early multi-nucleated cells; (2) asynchronous division/fusion of sub-nuclei of these multi-nucleated cells; (3) a series of polyploidising mitoses reverting replicative interphase from aborted metaphase and forming giant cells with a single nucleus; (4) micronucleation of arrested metaphases enclosing genome fragments; or (5) incomplete division in the multi-polar mitoses forming late multi-nucleated giant cells. We also observed that these activities can release para-diploid cells, although infrequently. While apoptosis typically occurs after a substantial delay in these cells, we also found that approximately 2% of the endopolyploid cells evade apoptosis and senescence arrest and continue some form of mitotic activity. We describe here that catalytically active Aurora-B kinase is expressed in the nuclei of many endopolyploid cells in interphase, as well as being present at the centromeres, mitotic spindle and cleavage furrow during their attempted mitotes. The totally micronucleated giant cells (containing sub-genomic fragments in multiple micronuclei) represented only the minor fraction which failed to undergo mitosis, and Aurora-B was absent from it. These observations suggest that most endopolyploid tumour cells are not reproductively inert and that Aurora-B may contribute to the establishment of resistant tumours post-irradiation.
    Citation
    Endopolyploidy in irradiated p53-deficient tumour cell lines: persistence of cell division activity in giant cells expressing Aurora-B kinase. 2008, 32 (9):1044-56 Cell Biol. Int.
    Journal
    Cell Biology International
    URI
    http://hdl.handle.net/10541/68735
    DOI
    10.1016/j.cellbi.2008.06.003
    PubMed ID
    18602486
    Type
    Article
    Language
    en
    ISSN
    1065-6995
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.cellbi.2008.06.003
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research
    School of Cancer and Imaging Sciences

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