1. Estrogen induces repression of the breast cancer and salivary gland expression gene in an estrogen receptor alpha-dependent manner
- Author
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Heike Brand, Stefanie Denger, Nicola Miller, Michael J. Kerin, Frank Gannon, Nancy Bretschneider, and Aoife Lowery
- Subjects
Hepatocyte Nuclear Factor 3-alpha ,Cancer Research ,medicine.medical_specialty ,Chromatin Immunoprecipitation ,medicine.drug_class ,Estrogen receptor ,promoters ,Down-Regulation ,Breast Neoplasms ,Biology ,Internal medicine ,Cell Line, Tumor ,medicine ,Biomarkers, Tumor ,Humans ,Promoter Regions, Genetic ,Estrogen receptor beta ,Regulation of gene expression ,Gene knockdown ,Binding Sites ,er-alpha ,Estrogen Receptor alpha ,Cancer ,Membrane Proteins ,foxa1 ,Estrogens ,medicine.disease ,proteins ,Neoplasm Proteins ,Gene Expression Regulation, Neoplastic ,Endocrinology ,Enhancer Elements, Genetic ,Oncology ,Estrogen ,Mutation ,Cancer research ,cells ,FOXA1 ,Estrogen receptor alpha ,reveals - Abstract
The focus of this study is on the expression and regulation of the estrogen-regulated breast cancer and salivary gland expression (BASE) gene that may function as a breast cancer marker. In MCF7 cells, BASE is repressed by estrogen in an estrogen receptor α (ERα)-dependent manner. Promoter analysis of the BASE gene led to the identification of a 2-kb upstream enhancer that harbors binding sites for ERα and FoxA1. The recruitment of both ERα and FoxA1 to this region was shown by chromatin immunoprecipitation analysis. Furthermore, mutation studies and knockdown experiments show a clear separation between gene expression mediated by FoxA1 and ERα-dependent gene regulation. Additionally, we provide information on BASE expression in human breast tumor samples. [Cancer Res 2008;68(1):106–14]
- Published
- 2008