Abstract | CONTEXT: OBJECTIVE: The aim of the study was to determine whether high levels of ERbeta in endometriotic stromal cells from ovarian endometriomas regulate ERalpha gene expression. RESULTS: CONCLUSIONS: High levels of ERbeta suppress ERalpha expression and response to estradiol in endometrial and endometriotic stromal cells via binding to classic and nonclassic DNA motifs in alternatively used ERalpha promoters. ERbeta also regulates cell cycle progression and might contribute to proliferation of endometriotic stromal cells. We speculate that a significantly increased ratio of ERbeta: ERalpha in endometriotic tissues may also suppress progesterone receptor expression and contribute to progesterone resistance. Thus, ERbeta may serve as a significant therapeutic target for endometriosis.
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Authors | Elena Trukhacheva, Zhihong Lin, Scott Reierstad, You-Hong Cheng, Magdy Milad, Serdar E Bulun |
Journal | The Journal of clinical endocrinology and metabolism
(J Clin Endocrinol Metab)
Vol. 94
Issue 2
Pg. 615-22
(Feb 2009)
ISSN: 0021-972X [Print] United States |
PMID | 19001520
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Chemical References |
- Estrogen Receptor alpha
- Estrogen Receptor beta
- RNA, Small Interfering
- Estradiol
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Topics |
- Adult
- Cell Cycle
(drug effects, genetics)
- Cells, Cultured
- Endometriosis
(genetics, metabolism, pathology)
- Estradiol
(pharmacology)
- Estrogen Receptor alpha
(genetics, metabolism)
- Estrogen Receptor beta
(antagonists & inhibitors, genetics, metabolism, physiology)
- Female
- Gene Expression Regulation
(drug effects)
- Humans
- Middle Aged
- Ovarian Diseases
(genetics, metabolism, pathology)
- Promoter Regions, Genetic
- Protein Binding
- RNA, Small Interfering
(pharmacology)
- Stromal Cells
(drug effects, metabolism, pathology)
- Transfection
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