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Role of direct interaction in BRCA1 inhibition of estrogen receptor activity
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Journal Article
Role of direct interaction in BRCA1 inhibition of estrogen receptor activity
2001
Overview
The BRCA1 gene was previously found to inhibit the transcriptional activity of the estrogen receptor [ER-alpha] in human breast and prostate cancer cell lines. In this study, we found that breast cancer-associated mutations of BRCA1 abolish or reduce its ability to inhibit ER-alpha activity and that domains within the amino- and carboxyl-termini of the BRCA1 protein are required for the inhibition. BRCA1 inhibition of ER-alpha activity was demonstrated under conditions in which a BRCA1 transgene was transiently or stably over-expressed in cell lines with endogenous wild-type BRCA1 and in a breast cancer cell line that lacks endogenous functional BRCA1 (HCC1937). In addition, BRCA1 blocked the expression of two endogenous estrogen-regulated gene products in human breast cancer cells: pS2 and cathepsin D. The BRCA1 protein was found to associate with ER-alpha in vivo and to bind to ER-alpha in vitro, by an estrogen-independent interaction that mapped to the amino-terminal region of BRCA1 (ca. amino acid 1-300) and the conserved carboxyl-terminal activation function [AF-2] domain of ER-alpha. Furthermore, several truncated BRCA1 proteins containing the amino-terminal ER-alpha binding region blocked the ability of the full-length BRCA1 protein to inhibit ER-alpha activity. Our findings suggest that the amino-terminus of BRCA1 interacts with ER-alpha, while the carboxyl-terminus of BRCA1 may function as a transcriptional repression domain. Oncogene (2001) 20, 77 - 87.
Publisher
Nature Publishing,Nature Publishing Group
Subject
/ Biological and medical sciences
/ Breast Neoplasms - metabolism
/ Estrogen
/ Fundamental and applied biological sciences. Psychology
/ Genes
/ Glutathione Transferase - genetics
/ Humans
/ Medicine
/ Molecular and cellular biology
/ Mutation
/ Oncology
/ Peptide Fragments - genetics
/ Peptide Fragments - metabolism
/ Proteins
/ Receptors, Estrogen - antagonists & inhibitors
/ Receptors, Estrogen - genetics
/ Receptors, Estrogen - metabolism
/ Recombinant Fusion Proteins - genetics
