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10.1038/ncomms10711

http://scihub22266oqcxt.onion/10.1038/ncomms10711
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C4756313!4756313!26876487
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suck abstract from ncbi


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pmid26876487      Nat+Commun 2016 ; 7 (ä): ä
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  • The histone variant H2A X is a regulator of the epithelial?mesenchymal transition #MMPMID26876487
  • Weyemi U; Redon CE; Choudhuri R; Aziz T; Maeda D; Boufraqech M; Parekh PR; Sethi TK; Kasoji M; Abrams N; Merchant A; Rajapakse VN; Bonner WM
  • Nat Commun 2016[]; 7 (ä): ä PMID26876487show ga
  • The epithelial?mesenchymal transition (EMT), considered essential for metastatic cancer, has been a focus of much research, but important questions remain. Here, we show that silencing or removing H2A.X, a histone H2A variant involved in cellular DNA repair and robust growth, induces mesenchymal-like characteristics including activation of EMT transcription factors, Slug and ZEB1, in HCT116 human colon cancer cells. Ectopic H2A.X re-expression partially reverses these changes, as does silencing Slug and ZEB1. In an experimental metastasis model, the HCT116 parental and H2A.X-null cells exhibit a similar metastatic behaviour, but the cells with re-expressed H2A.X are substantially more metastatic. We surmise that H2A.X re-expression leads to partial EMT reversal and increases robustness in the HCT116 cells, permitting them to both form tumours and to metastasize. In a human adenocarcinoma panel, H2A.X levels correlate inversely with Slug and ZEB1 levels. Together, these results point to H2A.X as a regulator of EMT.
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