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Endocrine-Related Cancer 12 (4) 851-866    DOI: 10.1677/erc.1.01039
Copyright © 2005 by the Society for Endocrinology.
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Estrogen receptor-{alpha} mediates gene expression changes and growth response in ovarian cancer cells exposed to estrogen

Amanda J M O’Donnell, Kenneth G Macleod, David J Burns, John F Smyth and Simon P Langdon

Cancer Research UK Centre, University of Edinburgh, Crewe Road South, Edinburgh EH4 2XR, UK

(Requests for offprints should be addressed to S Langdon; Email: simon.langdon{at}cancer.org.uk)

Estrogens play a significant role in the development, growth, invasion and metastasis of ovarian tumors. The transcriptional program regulated by 17ß-estradiol (E2) in human ovarian cancer cell lines was analyzed using cDNA microarrays containing 1200 cancer-related genes. Twenty-eight transcripts had at least a threefold change in expression in E2-treated PEO1 ovarian carcinoma cells compared with controls. These differences were confirmed by real-time quantitative PCR and shown to be dependent upon the expression of functional estrogen receptor-{alpha} (ER{alpha}). Consistent with this, these gene expression changes were blocked by the anti-estrogen tamoxifen. The use of ER{alpha}- and ERß-specific ligands allowed molecular dissection of the E2 response and showed that ER{alpha} activation was responsible for the observed changes in gene expression, whereas ERß played no significant role. Inhibition of de novo protein synthesis by cycloheximide was used to distinguish between primary and secondary target genes regulated by E2. Actinomycin D was used to show that changes in gene expression levels induced by E2 were a result of changes in transcription and not due to changes in mRNA stability. The results presented here demonstrate that estrogen-driven growth of epithelial ovarian carcinoma is mediated by activation of ER{alpha}-mediated, and not ERß-mediated, transcription.




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