ChIP-seq experiments of Estrogen Receptor Alpha (ERa) in the human breast cancer cell line T47D stably expressing GFP or neoGATA3. ChIP-seq experiments of Estrogen Receptor Alpha (ERa) in the human breast cancer cell line T47D stably expressing GFP or neoGATA3

In this study, we investigated the functions of the most common GATA3 mutation (X308_Splice) that we called “neoGATA3”. Analysis of available molecular data from >3000 breast cancer patients revealed a dysregulation of the ERa-dependent transcriptional response in tumors carrying this mutations. ChIP-Seq analysis indicated that ERa binding is reduced in neoGATA3-expressing cells, especially at distal regions, suggesting that neoGATA3 interferes with the fine-tuning of ERa-dependent gene expression.