Similar Datasets
Project description:We report changes in ER and GR binding profiles genome-wide upon co-treatment with Dex and E2 when compared to Dex or E2 treatments alone. We examine ER and GR binding under four different treatments (unt, Dex, E2, and Dex + E2).
2013-07-01 | E-GEOD-46123 | biostudies-arrayexpress
Project description:We report changes in ER and GR binding profiles genome-wide upon co-treatment with Dex and E2 when compared to Dex or E2 treatments alone.
2013-07-01 | GSE46123 | GEO
Project description:We report changes in DNaseI accessibility genome-wide upon co-treatment with Dex and E2 when compared to Dex or E2 treatments alone. We examine ER and GR binding under four different treatments (unt, Dex, E2, and Dex + E2).
2013-07-01 | E-GEOD-46121 | biostudies-arrayexpress
Project description:Analysis of MCF-7 cells treated for 4h with Ethanol, Estradiol (E2), Dexamethasone (Dex), or Estradiol + Dexamethasone (E2 + Dex) In estrogen receptor (ER)-negative breast cancer (BC), high tumor glucocorticoid receptor (GR) expression has been associated with a relatively poor outcome. In contrast, using a meta-analysis of several genomic datasets, here we find that tumor GR mRNA expression is associated with improved ER+ relapse-free survival (RFS) (independently of progesterone receptor (PR) expression). To understand the mechanism by which GR expression is associated with a better ER+ BC outcome, the global effect of GR-mediated transcriptional activation in ER+ BC cells was studied. Analysis of GR chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) in ER+/GR+ MCF-7 cells revealed that upon co-activation of GR and ER, GR chromatin association became enriched at proximal promoter regions. Furthermore, following ER activation, increased association of GR was observed at ER, FOXO, and AP1 response elements. In addition, it was determined that ER associated with GR response elements, suggesting that ER and GR interact in a complex. Co-activation of GR and ER resulted in increased expression (relative to ER activation alone) of transcripts that encode proteins promoting cellular differentiation (e.g. KDM4B, VDR) and inhibiting Wnt-signaling (IGFBP4). Finally, expression of these individual pro-differentiation genes was associated with significantly improved RFS in ER+ BC patients. Together, these data demonstrate that the co-expression and subsequent activity of tumor cell GR and ER contribute to the less aggressive natural history of early-stage BC by coordinating the altered expression of genes favoring differentiation. Four treatment samples (Vehicle V, Dex D, E2, or Dex+E2). Three biological replicate experiments per sample. Vehicle sample is Ethanol control.
2016-04-01 | E-GEOD-79761 | biostudies-arrayexpress
Project description:Analysis of MCF-7 cells treated for 4h with Ethanol, Estradiol (E2), Dexamethasone (Dex), or Estradiol + Dexamethasone (E2 + Dex) In estrogen receptor (ER)-negative breast cancer (BC), high tumor glucocorticoid receptor (GR) expression has been associated with a relatively poor outcome. In contrast, using a meta-analysis of several genomic datasets, here we find that tumor GR mRNA expression is associated with improved ER+ relapse-free survival (RFS) (independently of progesterone receptor (PR) expression). To understand the mechanism by which GR expression is associated with a better ER+ BC outcome, the global effect of GR-mediated transcriptional activation in ER+ BC cells was studied. Analysis of GR chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq) in ER+/GR+ MCF-7 cells revealed that upon co-activation of GR and ER, GR chromatin association became enriched at proximal promoter regions. Furthermore, following ER activation, increased association of GR was observed at ER, FOXO, and AP1 response elements. In addition, it was determined that ER associated with GR response elements, suggesting that ER and GR interact in a complex. Co-activation of GR and ER resulted in increased expression (relative to ER activation alone) of transcripts that encode proteins promoting cellular differentiation (e.g. KDM4B, VDR) and inhibiting Wnt-signaling (IGFBP4). Finally, expression of these individual pro-differentiation genes was associated with significantly improved RFS in ER+ BC patients. Together, these data demonstrate that the co-expression and subsequent activity of tumor cell GR and ER contribute to the less aggressive natural history of early-stage BC by coordinating the altered expression of genes favoring differentiation.
2016-04-01 | GSE79761 | GEO
Project description:Steroid hormone receptors are simultaneously active in many tissues and capable of altering each other's function. Estrogen receptor ɑ (ER) and glucocorticoid receptor (GR) are expressed in the uterus and their ligands have opposing effects on uterine growth. In endometrial tumors expressing high levels of ER, 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 significantly altered 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 novel regulated genes. Our results suggest phenotypic and molecular interplay between ER and GR in endometrial cancer.
2018-03-13 | GSE109891 | GEO
Project description:Steroid hormone receptors are simultaneously active in many tissues and capable of altering each other's function. Estrogen receptor ɑ (ER) and glucocorticoid receptor (GR) are expressed in the uterus and their ligands have opposing effects on uterine growth. In endometrial tumors expressing high levels of ER, 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 significantly altered 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 novel regulated genes. Our results suggest phenotypic and molecular interplay between ER and GR in endometrial cancer.
2018-03-13 | GSE109890 | GEO
Project description:Exploring effect of estrogen and progesterone/progestin treatment on ER and PR binding. Two cell lines, four conditions (Vehicle, E2, Progesterone, E2+Progesterone), three factors (ER, PR, p300), all with three replicates.
2015-05-22 | E-GEOD-68356 | biostudies-arrayexpress
Project description:Using scaling from PhysB model
Blood flow in L/hr
Compartments in Kg
Baseline as ~0.013nM free E2 in plasma_venous
E2 biosynthesis rate constant = 2
E2 biosynthesis species = 1nM
CLeh = 5
CLint = 1scaled by liver weight
B:P = 0.286
IV bolus = 250/h (delivers in 2-3mins)
Added ER{gonads}
2018-02-02 | MODEL1711210001 | BioModels
Project description:Exploring effect of progesterone/progestin treatment on ER and PR binding. Two cell lines, three conditions (Full Media with E2, E2+ Progesterone, Full Media + R5020 Progestin), three factors (ER, PR, p300), all with three replicates, each with a matched Input control.
2015-05-22 | E-GEOD-68355 | biostudies-arrayexpress