Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Glucocorticoid Receptor Action in Breast Cancer

ABSTRACT: Glucocorticoid Receptor Action in Breast Cancer

PROVIDER: PRJNA923379 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23061264_1.fastq.gz	Fastqsanger.gz
	SRR23061264_2.fastq.gz	Fastqsanger.gz
	SRR23061265_1.fastq.gz	Fastqsanger.gz
	SRR23061265_2.fastq.gz	Fastqsanger.gz
	SRR23061266_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 34

Similar Datasets

Glucocorticoid Receptor Action in Breast Cancer [ChIP-Seq]

Project description:Glucocorticoid Receptor Action in Breast Cancer [ChIP-Seq]

| PRJNA923381 | ENA

Glucocorticoid Receptor Action in Breast Cancer [RNA-Seq]

Project description:Glucocorticoid Receptor Action in Breast Cancer [RNA-Seq]

| PRJNA923273 | ENA

Glucocorticoid Receptor Action in Breast Cancer [ChIP-Seq]

Project description:Various omics datastreams related to mechanisms underlying glucocorticoid receptor action in breast cancer cells - we performed mRNA sequencing and ER/GR-ChIP sequencing.

2023-10-02 | GSE222798 | GEO

Glucocorticoid Receptor Action in Breast Cancer [RNA-Seq]

Project description:Various omics datastreams related to mechanisms underlying glucocorticoid receptor action in breast cancer cells - we performed mRNA sequencing and ER/GR-ChIP sequencing.

2023-10-02 | GSE222728 | GEO

Breast cancer identity is determined by glucocorticoid receptor activity status

Project description:Glucocorticoid receptor (GR) is a ligand-inducible transcription factor with an intricate role in cancer biology. Using an in silico designed GR activity signature we show that GR is a tumor suppressor across diverse primary cancers. In breast cancer, GR activity status determines luminal identity, and importantly, relates to patients’ outcomes. We illustrate that GR suppresses tumor growth, mediated through its engagement with the estrogen receptor-α (ER). This steroid hormone receptor cross-talk leads to redistribution of ERα on chromatin, ultimately leading to expression of ZBTB16 gene. We define ZBTB16 as a transcriptional repressor and a tumor suppressor in ER-positive breast cancer. Importantly, highly aggressive ER-positive breast cancer cells displaying absence of GR activity can be eradicated if GR-induced gene repression is mimicked by inhibitors of the epigenetic pathway. In line with this, epigenetic regulators are highly expressed upon GR activity loss, leading to vulnerability of aggressive breast cancer cells to clinically available epigenetic inhibitors. Our findings indicate that GR functions as a tumor suppressor by repositioning ER to specific sites on chromatin, modulating targetable pathways, which has important implications for patients’ prognosis and therapeutic interventions.

2023-10-02 | PXD039209 | Pride

Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer

Project description:Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer

| PRJNA887022 | ENA

Ligand-dependent genomic function of glucocorticoid receptor in triple-negative breast cancer

Project description:Glucocorticoids (GC) have been widely used as coadjuvants in the treatment of solid tumors, but GC treatment may be associated with poor pharmacotherapeutic response and/or prognosis. The genomic action of GC in these tumors is largely unknown. Here we find that dexamethasone (Dex, a synthetic GC) regulated genes in triple-negative breast cancer (TNBC) cells are associated with drug resistance. Importantly, these GC-regulated genes are aberrantly expressed in TNBC patients and associated with unfavorable clinical outcomes. Interestingly, in TNBC cells, Compound A (CpdA, a selective GR modulator) only regulates a small number of genes not involved in carcinogenesis and therapy resistance. Mechanistic studies using a ChIP-exo approach reveal that Dex- but not CpdA-liganded glucocorticoid receptor (GR) binds to a single glucocorticoid response element (GRE), which drives the expression of pro-tumorigenic genes. Our data suggest that development of safe coadjuvant therapy should consider the distinct genomic function between Dex- and CpdA-liganded GR. To study GR-regulated genes and define GRE in human genome, RNA-seq and GR ChIP-exo are performed in MDA-MB-231 cells before/after dex and CpdA stimulation. Each experiment includes two replicates.

2015-09-18 | E-GEOD-56022 | biostudies-arrayexpress

Glucocorticoid receptor axis in lung cancer

Project description:Glucocorticoid receptor axis in lung cancer

| PRJNA669682 | ENA

The Glucocorticoid Receptor Interferes with Progesterone Receptor-Dependent Genomic Regulation in Breast Cancer Cells

Project description:The Glucocorticoid Receptor Interferes with Progesterone Receptor-Dependent Genomic Regulation in Breast Cancer Cells

| PRJNA523539 | ENA

Ligand-dependent genomic function of glucocorticoid receptor in triple-negative breast cancer

2015-09-18 | GSE56022 | GEO