ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR180/005/SRR1802085/SRR1802085.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR180/004/SRR1802084/SRR1802084.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR180/000/SRR1802080/SRR1802080.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR180/001/SRR1802081/SRR1802081.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR180/008/SRR1802078/SRR1802078.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR180/009/SRR1802079/SRR1802079.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR180/003/SRR1802083/SRR1802083.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR180/002/SRR1802082/SRR1802082.fastq.gzprimary200OKGenomicsDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingenhttps://www.ebi.ac.uk/ena/browser/view/PRJNA275306Homo sapiensxref:PubMed:25788266Hormone-dependent gene expression requires dynamic and coordinated epigenetic changes. Estrogen receptor-positive (ER+) breast cancer is particularly dependent upon extensive chromatin remodeling and changes in histone modifications for the induction of hormone-responsive gene expression. Our previous studies established an important role of bromodomain-containing protein-4 (BRD4) in promoting estrogen-regulated transcription and proliferation of ER+ breast cancer cells. Here, we investigated the association between genome-wide occupancy of histone H4 acetylation at lysine 12 (H4K12ac) and BRD4 in the context of estrogen-induced transcription. Similar to BRD4, we observed that H4K12ac occupancy increases near the transcription start sites (TSS) of estrogen-induced genes as well as at distal ERα binding sites in an estrogen-dependent manner. Interestingly, H4K12ac occupancy highly correlates with BRD4 binding and enhancer RNA production on ERα-positive enhancers. Consistent with an importance in estrogen-induced gene transcription, H4K12ac occupancy globally increased in ER-positive cells relative to ER-negative cells and these levels were further increased by estrogen treatment in an ERα-dependent manner. Together, these findings reveal a strong correlation between H4K12ac and BRD4 occupancy with estrogen-dependent gene transcription and further suggest that modulators of H4K12ac and BRD4 may serve as new therapeutic targets for hormone-dependent cancers. Overall design: ChIP-seq profiles of H4K12ac in MCF7 cells treated with +/- estrogen treatment and MCF10A cells.ENAfalseHomo sapiensH4K12ac is regulated by estrogen receptor-alpha and is associated with BRD4 function and inducible transcription2025-09-242015-05-04PRJNA275306GSE65886960625788266