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Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE109893 | GEO | 2018/03/13

REPOSITORIES: GEO

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Clinical and Genomic Crosstalk between Glucocorticoid Receptor and Estrogen Receptor ? In Endometrial Cancer.

Project description:Steroid hormone receptors are simultaneously active in many tissues and are capable of altering each other's function. Estrogen receptor ? (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.

| S-EPMC5870123 | biostudies-literature

Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer [ChIP-seq]

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

Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer [ATAC-seq]

2018-03-13 | GSE109890 | GEO

Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer [RNA-seq]

2018-03-13 | GSE109892 | GEO

Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer

Project description:Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer

| PRJNA432243 | ENA

Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer [ChIP-seq]

Project description:Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer [ChIP-seq]

| PRJNA432244 | ENA

Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer [ATAC-seq]

Project description:Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer [ATAC-seq]

| PRJNA432246 | ENA

Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer [RNA-seq]

Project description:Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer [RNA-seq]

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Estrogen receptor α wields treatment-specific enhancers between morphologically similar endometrial tumors.

Project description:The DNA-binding sites of estrogen receptor α (ERα) show great plasticity under the control of hormones and endocrine therapy. Tamoxifen is a widely applied therapy in breast cancer that affects ERα interactions with coregulators and shifts the DNA-binding signature of ERα upon prolonged exposure in breast cancer. Although tamoxifen inhibits the progression of breast cancer, it increases the risk of endometrial cancer in postmenopausal women. We therefore asked whether the DNA-binding signature of ERα differs between endometrial tumors that arise in the presence or absence of tamoxifen, indicating divergent enhancer activity for tumors that develop in different endocrine milieus. Using ChIP sequencing (ChIP-seq), we compared the ERα profiles of 10 endometrial tumors from tamoxifen users with those of six endometrial tumors from nonusers and integrated these results with the transcriptomic data of 47 endometrial tumors from tamoxifen users and 64 endometrial tumors from nonusers. The ERα-binding sites in tamoxifen-associated endometrial tumors differed from those in the tumors from nonusers and had distinct underlying DNA sequences and divergent enhancer activity as marked by histone 3 containing the acetylated lysine 27 (H3K27ac). Because tamoxifen acts as an agonist in the postmenopausal endometrium, similar to estrogen in the breast, we compared ERα sites in tamoxifen-associated endometrial cancers with publicly available ERα ChIP-seq data in breast tumors and found a striking resemblance in the ERα patterns of the two tissue types. Our study highlights the divergence between endometrial tumors that arise in different hormonal conditions and shows that ERα enhancer use in human cancer differs in the presence of nonphysiological endocrine stimuli.

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Genomics of signaling crosstalk of estrogen receptor alpha in breast cancer cells.

Project description:BACKGROUND: The estrogen receptor alpha (ERalpha) is a ligand-regulated transcription factor. However, a wide variety of other extracellular signals can activate ERalpha in the absence of estrogen. The impact of these alternate modes of activation on gene expression profiles has not been characterized. METHODOLOGY/PRINCIPAL FINDINGS: We show that estrogen, growth factors and cAMP elicit surprisingly distinct ERalpha-dependent transcriptional responses in human MCF7 breast cancer cells. In response to growth factors and cAMP, ERalpha primarily activates and represses genes, respectively. The combined treatments with the anti-estrogen tamoxifen and cAMP or growth factors regulate yet other sets of genes. In many cases, tamoxifen is perverted to an agonist, potentially mimicking what is happening in certain tamoxifen-resistant breast tumors and emphasizing the importance of the cellular signaling environment. Using a computational analysis, we predicted that a Hox protein might be involved in mediating such combinatorial effects, and then confirmed it experimentally. Although both tamoxifen and cAMP block the proliferation of MCF7 cells, their combined application stimulates it, and this can be blocked with a dominant-negative Hox mutant. CONCLUSIONS/SIGNIFICANCE: The activating signal dictates both target gene selection and regulation by ERalpha, and this has consequences on global gene expression patterns that may be relevant to understanding the progression of ERalpha-dependent carcinomas.

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