Journal
CELL REPORTS
Volume 22, Issue 11, Pages 2995-3005Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.02.076
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Funding
- NIH/National Human Genome Research Institute (NHGRI) [R00 HG006922]
- NIH/NHGRI [R01 HG008974]
- Huntsman Cancer Institute
- Women's Cancers Disease-Oriented Team at the Huntsman Cancer Institute
- NIH/National Cancer Institute [P30 CA042014]
- [R00 HG006922S1]
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Steroid hormone receptors are simultaneously active in many tissues and are capable of altering each other's function. Estrogen receptor a (ER) and glucocorticoid receptor (GR) are expressed in the uterus, and their ligands have opposing effects on uterine growth. In endometrial tumors with high ER expression, we surprisingly found that expression of GR is associated with poor prognosis. Dexamethasone reduced normal uterine growth in vivo; however, this growth inhibition was abolished in estrogen-induced endometrial hyperplasia. We observed low genomic-binding site overlap when ER and GR are induced with their respective ligands; however, upon simultaneous induction they co-occupy more sites. GR binding is altered significantly by estradiol with GR recruited to ER-bound loci that become more accessible upon estradiol induction. Gene expression responses to co-treatment were more similar to estradiol but with additional regulated genes. Our results suggest phenotypic and molecular interplay between ER and GR in endometrial cancer.
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