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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.