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- W3205067513 abstract "6123 Of the hereditary breast cancers, only 40-45% can be attributed to mutations in the BRCA-1 coding sequence. While the coding sequence is rarely mutated in sporadic breast cancer, reduced levels of wild-type BRCA-1 protein are often found in these tumors suggesting that non-mutational events, such as environmental insults may lower the expression of BRCA-1. Our investigations of the BRCA-1 promoter revealed consensus sequences for activator protein-1 (AP-1 = 5’-CTGAG-3’) and xenobiotic responsive element (XRE = 5’-GCGTG-3’). In transient transfection studies, we found that estrogen induced transcription activity of a 1.7 kb BRCA-1 promoter fragment containing the transcriptional start sites for exon 1A and 1B. Using chromatin immunoprecipitation (ChIP) assays, we found that estrogen stimulated the recruitment of c-Jun, FosB, Fra-2 and the estrogen receptor-α (ERα) and the cofactor p300 at a 237 bp promoter fragment upstream of exon 1B comprising the AP-1 element. The cotreatment with tamoxifen antagonized the recruitment of p300 and ERα to this region. Results of electromobility shift assays mapped the binding site for the ERα to a 32 bp region (-46 to -14) comprising the candidate AP-1 motif. These results support a model in which estrogen activation of BRCA-1 transcription requires the formation of an AP-1/ERα complex containing the cofactor p300. In addition, site-directed mutagenesis of the XRE site resulted in loss of estrogen stimulation of BRCA-1 expression suggesting that the XRE may act as a positive regulator of estrogen regulation of BRCA-1. ChIP assays confirmed the recruitment of the aromatic hydrocarbon receptor (AhR) to a promoter fragment containing the XRE. The recruitment of the ERα and AhR respectively to the AP-1 and XRE sites is time dependent and follows a cyclical pattern. We propose that the unliganded AhR is required for estrogen induction of BRCA-1 transcription. Conversely, ligands of the AhR may repress BRCA-1 transcription possibly by stimulating competition of the AhR with the ERα for common transcription factors. A potential contribution of these findings is an increased understanding of the mechanistic pathway in which ligands of the AhR can influence BRCA-1 expression and contribute to the etiology of sporadic breast cancer." @default.
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- W3205067513 date "2005-05-01" @default.
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- W3205067513 title "Requirement of the estrogen receptor-α and aromatic hydrocarbon receptor in transcriptional regulation of BRCA-1" @default.
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