Segregation of Steroid Receptor Coactivator-1 from Steroid Receptors in Mammary Epithelium

• Published in: Proceedings of the National Academy of Sciences - PNAS 1999-01, Vol.96 (1), p.208-213
• Main Authors: Shim, Woo-Shin, DiRenzo, James, DeCaprio, James A., Santen, Richard J., Brown, Myles, Jeng, Meei-Huey
• Format: Article
• Language: English
• Subjects: Animals; Antibodies; Biological Sciences; Cell separation; Cellular immunity; Epithelial cells; Epithelial Cells - chemistry; Epithelium; Estrogens; Estrogens - pharmacology; Female; Gene Expression; Genes; Histone Acetyltransferases; Hormones; Immunohistochemistry; L cells; Mammary glands; Mammary Glands, Animal - chemistry; Mammary Glands, Animal - drug effects; Medical research; Nuclear Receptor Coactivator 1; Proteins; Rats; Rats, Sprague-Dawley; Receptors, Estrogen - isolation & purification; Receptors, Progesterone - isolation & purification; Receptors, Steroid - isolation & purification; Steroid receptors; Steroids; Stromal cells; Stromal Cells - chemistry; Transcription Factors - isolation & purification
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.96.1.208

Steroid receptor coactivator-1 (SRC-1) family members interact with steroid receptors, including estrogen receptor α (ERα) and progesterone receptor (PR), to enhance ligand-dependent transcription. However, the expression of ERα and SRC-1 was found to be segregated in distinct subsets of cells within the epithelium of the estrogen-responsive rat mammary gland. This finding was in contrast to the finding for the stroma, where significant numbers of cells coexpressed ERα and SRC-1. Treatment of animals with estrogen induced PR expression in the ERα -expressing mammary epithelial cells in the absence of detectable SRC-1 and did not affect the segregated pattern of SRC-1 and ERα expression. PR was neither expressed nor induced by estrogen treatment in stroma, despite the coexpression of ERα and SRC-1. These results suggest that SRC-1 is not necessary for ERα -mediated induction of PR in mammary epithelial cells and is also not sufficient for PR induction in stromal cells expressing both ERα and SRC-1. Furthermore, the expression of SRC-1 in a subpopulation of mammary epithelial cells distinct from those expressing ERα or PR raises the possibility that SRC-1 has cell type-specific functions other than simply to act as coactivator for ERα or PR in the mammary epithelium.