Details

Autor(en) / Beteiligte

• Weyemi, Urbain
• Redon, Christophe E
• Choudhuri, Rohini
• Aziz, Towqir
• Maeda, Daisuke
• Boufraqech, Myriem
• Parekh, Palak R
• Sethi, Taresh K
• Kasoji, Manjula
• Abrams, Natalie
• Merchant, Anand
• Rajapakse, Vinodh N
• Bonner, William M

Titel

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

Ist Teil von

• Nature communications, 2016-02, Vol.7 (1), p.10711-10711, Article 10711

Ort / Verlag

England: Nature Publishing Group

Erscheinungsjahr

2016

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• 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.