The histone variant H2A.X is a regulator of the epithelial–mesenchymal transition

Urbain Weyemi (), Christophe E. Redon, Rohini Choudhuri, Towqir Aziz, Daisuke Maeda, Myriem Boufraqech, Palak R. Parekh, Taresh K. Sethi, Manjula Kasoji, Natalie Abrams, Anand Merchant, Vinodh N. Rajapakse and William M. Bonner ()
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Urbain Weyemi: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
Christophe E. Redon: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
Rohini Choudhuri: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
Towqir Aziz: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
Daisuke Maeda: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
Myriem Boufraqech: Endocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health
Palak R. Parekh: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
Taresh K. Sethi: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
Manjula Kasoji: Center for Cancer Research Collaborative Bioinformatics Resource, National Cancer Institute
Natalie Abrams: Center for Cancer Research Collaborative Bioinformatics Resource, National Cancer Institute
Anand Merchant: Center for Cancer Research Collaborative Bioinformatics Resource, National Cancer Institute
Vinodh N. Rajapakse: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
William M. Bonner: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: Abstract 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.

Date: 2016
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DOI: 10.1038/ncomms10711

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