Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA432243 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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]

| PRJNA432245 | 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 [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 [RNA-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 | GSE109892 | GEO

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

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

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

Exploiting crosstalk between glucocorticoid and mineralocorticoid receptors enhances glucocorticoid-induced killing of multiple myeloma cells

Project description:Long-term glucocorticoid treatment in multiple myeloma is hampered by deleterious side effects. Glucocorticoids bind to the glucocorticoid receptor (GR), which is a crucial drug target because its activation triggers myeloma cell death. The mineralocorticoid receptor (MR) is a closely related nuclear receptor but its impact on glucocorticoid responsiveness in myeloma is unknown. Here we reveal a functional crosstalk between GR and 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 enhances Dex-induced cell killing in (primary) myeloma cells. The crosstalk is further evidenced by an endogenous interaction between GR and MR in myeloma cells that is ligand-inducible and by a distinctive gene expression profile. Our study demonstrates that GR-MR crosstalk is therapeutically relevant in myeloma and presents a glucocorticoid-based dose-reduction strategy that could diminish glucocorticoid-related side effects in patients.

2023-08-23 | GSE200313 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data