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    Up-regulation of the embryonic self-renewal network through reversible polyploidy in irradiated p53-mutant tumour cells.

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    Authors
    Salmina, Kristine
    Jankevics, Eriks
    Huna, Anda
    Perminov, Dmitry
    Radovica, Ilze
    Klymenko, Tetyana
    Ivanov, Andrei
    Jascenko, Elina
    Scherthan, Harry
    Cragg, Mark S
    Erenpreisa, Jekaterina
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    Affiliation
    Latvian Biomedical Research and Study Centre, Riga, LV-1067, Latvia. kristine@biomed.lu.lv
    Issue Date
    2010-08-01
    
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    Abstract
    We have previously documented that transient polyploidy is a potential cell survival strategy underlying the clonogenic re-growth of tumour cells after genotoxic treatment. In an attempt to better define this mechanism, we recently documented the key role of meiotic genes in regulating the DNA repair and return of the endopolyploid tumour cells (ETC) to diploidy through reduction divisions after irradiation. Here, we studied the role of the pluripotency and self-renewal stem cell genes NANOG, OCT4 and SOX2 in this polyploidy-dependent survival mechanism. In irradiation-resistant p53-mutated lymphoma cell-lines (Namalwa and WI-L2-NS) but not sensitive p53 wild-type counterparts (TK6), low background expression of OCT4 and NANOG was up-regulated by ionising radiation with protein accumulation evident in ETC as detected by OCT4/DNA flow cytometry and immunofluorescence (IF). IF analysis also showed that the ETC generate PML bodies that appear to concentrate OCT4, NANOG and SOX2 proteins, which extend into complex nuclear networks. These polyploid tumour cells resist apoptosis, overcome cellular senescence and undergo bi- and multi-polar divisions transmitting the up-regulated OCT4, NANOG and SOX2 self-renewal cassette to their descendents. Altogether, our observations indicate that irradiation-induced ETC up-regulate key components of germ-line cells, which potentially facilitate survival and propagation of the tumour cell population.
    Citation
    Up-regulation of the embryonic self-renewal network through reversible polyploidy in irradiated p53-mutant tumour cells. 2010, 316 (13):2099-112 Exp Cell Res
    Journal
    Experimental Cell Research
    URI
    http://hdl.handle.net/10541/111380
    DOI
    10.1016/j.yexcr.2010.04.030
    PubMed ID
    20457152
    Type
    Article
    Language
    en
    ISSN
    0014-4827
    EISSN
    1090-2422
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.yexcr.2010.04.030
    Scopus Count
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    All Paterson Institute for Cancer Research

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