ChIP-seq profiling of estrogen receptor binding in MCF-7 cells exposed to 5a-DTT, Flutamide, Estradiol, and Bisphenol B

Endocrine-disrupting chemicals (EDCs) can modulate estrogen receptor (ER) signaling by altering its transcriptional activity. To investigate these effects, we performed chromatin immunoprecipitation sequencing (ChIP-seq) on cells treated with 5a-Dihydrotestosterone (5a-DTT), Flutamide, Estradiol, and Bisphenol B. This dataset includes raw sequencing reads, processed peak files, and metadata, enabling the identification of ER binding sites influenced by each EDC. Gene ontology (GO) analysis of ChIP-enriched regions revealed that these compounds affect key pathways, including antibody-dependent cytotoxicity, BMP signaling in cardiac induction, and hepatocyte growth factor receptor signaling. This dataset provides insights into EDC-induced transcriptional regulation and contributes to the understanding of their role in endocrine disruption. Overall design: This study analyzes the effects of endocrine-disrupting chemicals (EDCs) binding to the estrogen receptor (ER) in MCF-7 cells and how this binding influences subsequent ER-DNA interactions using ChIP-seq. Cells were treated with four different EDCs: 5a-Dihydrotestosterone (5a-DTT), Flutamide, Estradiol, and Bisphenol B. ChIP was performed using an anti-ER antibody to capture ER-bound chromatin, followed by high-throughput sequencing. This dataset provides insights into EDC-induced transcriptional regulation and ER-DNA interactions.