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

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

PROVIDER: PRJNA432246 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6653441.fastq.gz	Fastqsanger.gz
	SRR6653442.fastq.gz	Fastqsanger.gz
	SRR6653443.fastq.gz	Fastqsanger.gz
	SRR6653444.fastq.gz	Fastqsanger.gz

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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

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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]

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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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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]

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Knockdown of mineralocorticoid receptor or glucocorticoid receptor on human endometrial stromal cells and decidualization

Project description:To clarify mineralcorticoid receptor and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells.

2012-11-28 | GSE42538 | GEO

Knockdown of mineralocorticoid receptor or glucocorticoid receptor on human endometrial stromal cells and decidualization

Project description:To clarify mineralcorticoid receptor and glucocorticoid receptor-dependent gene networks in decidualizing human endometrial stromal cells. Genome-wide microarray analysis was performed on primary cultures established from 4 different patients. Stromal cell cultures were subjected to either GR or MR siRNA knockdown or control non-targeting siRNA then decidualized for four days before harvesting and RNA extraction for microarray analysis.

2012-11-28 | E-GEOD-42538 | biostudies-arrayexpress

Crosstalk between the glucocorticoid and mineralocorticoid receptor boosts glucocorticoid-induced killing of multiple myeloma cells

Project description:The glucocorticoid receptor (GR) is a crucial drug target in multiple myeloma as its activation with glucocorticoids effectively triggers myeloma cell death. However, as high-dose glucocorticoids are also associated with deleterious side effects, novel approaches are urgently needed to improve GR’s action in myeloma. Here we reveal a functional crosstalk between GR and the mineralocorticoid receptor (MR) that culminates in improved myeloma cell killing. We show that the GR agonist Dexamethasone (Dex) downregulates MR levels in a GR-dependent way in myeloma cells. Co-treatment of Dex with the MR antagonist Spironolactone (Spi) enhances Dex-induced cell killing in primary, newly diagnosed GC-sensitive myeloma cells, while in a relapsed GC-resistant setting, Spi alone induces distinct myeloma cell killing. On a mechanistic level, we find that a GR-MR crosstalk is arising from an endogenous interaction between GR and MR in myeloma cells. Quantitative dimerization assays show that Spi reduces Dex-induced GR-MR heterodimerization and completely abolishes Dex-induced MR MR homodimerization but leaves GR-GR homodimerization intact. Unbiased transcriptomics further reveals that c-myc and many of its target genes are downregulated most by Dex and Spi combined, while proteomics analyses identify that several metabolic hallmarks are modulated most by this combination treatment. Finally, we identified a subset of Dex+Spi downregulated genes and proteins that may predict prognosis in the CoMMpass patient cohort. Our study demonstrates that GR-MR crosstalk is therapeutically relevant in myeloma as it provides novel strategies towards glucocorticoid-based dose-reduction.

2023-10-24 | PXD043635 | Pride

Aberrant claudin-6–adhesion signal promotes endometrial cancer progression via estrogen receptor α

Project description:Cell adhesion proteins not only maintain tissue integrity but also possess signaling abilities to organize diverse cellular events in a variety of physiological and pathological processes; however, the underlying mechanism remains obscure. Among cell adhesion molecules, the claudin (CLDN) family often possesses aberrant expression in various cancers, but the biological relevance and molecular basis have not yet been established. Here, we show that high CLDN6 expression accelerates cellular proliferation and migration in human endometrial cancer cells in vitro. Using xenograft model, we also revealed that aberrant CLDN6 expression promotes tumor growth and invasion in endometrial cancer tissues. The second extracellular domain and Y196/200 of CLDN6 were required to recruit and activate Src-family kinases (SFKs) and to stimulate malignant phenotypes. Importantly, we demonstrate that the CLDN6/SFK/PI3K-dependent AKT and SGK (serum- and glucocorticoid-regulated kinase) signalings target Ser518 in the human estrogen receptor α and ligand-independently activate target genes in endometrial cancer cells, resulting in cancer development. CLDN6, at least in part, also regulated gene expression in an ERα-independent manner.

2021-03-20 | GSE161384 | GEO

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