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

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

PROVIDER: PRJNA523539 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8601860.fastq.gz	Fastqsanger.gz
	SRR8601870.fastq.gz	Fastqsanger.gz
	SRR8601851.fastq.gz	Fastqsanger.gz
	SRR8601861.fastq.gz	Fastqsanger.gz
	SRR8601871.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Project description:The glucocorticoid and progesterone receptors (GR and PR) are closely related members of the steroid receptor family. Despite sharing similar structural and functional characteristics; the cognate hormones display very distinct physiological responses. In mammary epithelial cells, PR activation is associated with the incidence and progression of breast cancer, whereas the GR is related to growth suppression and differentiation. Despite their pharmacological relevance, only a few studies have compared GR and PR activities in the same system. Using a PR+/GR+ breast cancer cell line, here we report that either glucocorticoid-free or dexamethasone-activated GR inhibits progestin-dependent gene expression associated to epithelial-mesenchymal-transition and cell proliferation. When both receptors are activated with their cognate hormones, PR and GR can form part of the same complex according to co-immunoprecipitation, quantitative microscopy, and sequential ChIP experiments. Moreover, genome-wide studies in cells treated with either dexamethasone or R5020, revealed the presence of several regions co-bound by both receptors. Surprisingly, GR also binds novel genomic sites in cells treated with R5020 alone. This progestin-induced GR binding was enriched in REL DNA motifs and located close to genes coding for chromatin remodelers. Understanding GR behavior in the context of progestin-dependent breast cancer could provide new targets for tumor therapy.

2019-11-25 | GSE126859 | GEO

The glucocorticoid receptor interferes with progesterone receptor-dependent genomic regulation in breast cancer cells.

Project description:The glucocorticoid and progesterone receptors (GR and PR) are closely related members of the steroid receptor family. Despite sharing similar structural and functional characteristics; the cognate hormones display very distinct physiological responses. In mammary epithelial cells, PR activation is associated with the incidence and progression of breast cancer, whereas the GR is related to growth suppression and differentiation. Despite their pharmacological relevance, only a few studies have compared GR and PR activities in the same system. Using a PR+/GR+ breast cancer cell line, here we report that either glucocorticoid-free or dexamethasone (DEX)-activated GR inhibits progestin-dependent gene expression associated to epithelial-mesenchymal-transition and cell proliferation. When both receptors are activated with their cognate hormones, PR and GR can form part of the same complex according to co-immunoprecipitation, quantitative microscopy and sequential ChIP experiments. Moreover, genome-wide studies in cells treated with either DEX or R5020, revealed the presence of several regions co-bound by both receptors. Surprisingly, GR also binds novel genomic sites in cells treated with R5020 alone. This progestin-induced GR binding was enriched in REL DNA motifs and located close to genes coding for chromatin remodelers. Understanding GR behavior in the context of progestin-dependent breast cancer could provide new targets for tumor therapy.

| S-EPMC6846950 | biostudies-literature

Glucocorticoid Receptor Action in Breast Cancer

Project description:Glucocorticoid Receptor Action in Breast Cancer

| PRJNA923379 | ENA

Fasting boosts breast cancer therapy via glucocorticoid activation.

Project description:The vast majority of all breast cancers are driven by oestrogen receptor alpha (ERα) activation, and endocrine therapy represents the mainstay treatment for these patients. However, resistance is common and tumours progress despite years of systemic endocrine suppression. Periodic fasting enhances the efficacy of standard endocrine drugs and delay acquired resistance to them, although the underlying mechanisms remain unclear. Here, we show that fasting, in combination with endocrine therapy, induces extensive epigenetic reprogramming in hormone receptor-positive (HR+) breast cancer xenografts, with large-scale activation of glucocorticoid receptor (GR) and progesterone receptor (PR) signalling, and impairment of activator protein-1 (AP-1) family activity. GR-driven gene programs were selectively activated after fasting, and GR knockout perturbed the beneficial effects of fasting in combination with tamoxifen, in vivo. Exogenous administration of GR-ligands fully recapitulated the observed fasting-enhanced anti-oestrogen action, resulting in tumour regression. Finally, elevated progesterone and cortisol levels were detected in the blood of breast cancer patients after fasting, thus providing clinical validation of our animal findings. Our results indicate GR activation to play a pivotal role in fasting’s ability to enhance endocrine drug activity against hormone-receptor positive breast cancer and suggest that corticosteroid administration should be evaluated as an adjuvant to endocrine therapy in this condition.

2025-10-14 | PXD049477 | Pride

Differential regulation of SGK1 by progesterone activates AP-1/NDRG1 genomic axis in PR-positive and negative breast cancer cells

Project description:Pre-operative progesterone intervention has been shown to confer a survival benefit to breast cancer patients independent of their progesterone receptor (PR) status, raising a question about how progesterone affects the outcome of PR-negative cells. Here, we identify up-regulation of a Serum- and glucocorticoid-regulated kinase gene, SGK1 and an N-Myc Downstream Regulated Gene 1, NDRG1, along with down-regulation of miR-29a and miR-101-1 targeting 3’UTR region of SGK1, to differential extents in a PR dependent manner in breast cancer cells. We further demonstrate a novel dual-phase transcriptional and post-transcriptional regulation of SGK1 in response to progesterone leading to up-regulation of a tumor metastasis suppressor gene, NDRG1, mediated by a set of AP-1 network genes. The NDRG1 further inactivates a set of kinases impeding the invasion and migration of breast cancer cells. In summary, we propose a model for the mode of action of progesterone in breast cancer deciphering the molecular basis of a randomized clinical trial studying the effect of progesterone in breast cancer with a potential to improve the prognosis of breast cancer patients for receiving pre-operative progesterone treatment.

2018-10-19 | E-MTAB-6742 | biostudies-arrayexpress

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

| PRJNA923381 | ENA

MicroRNA signatures predict Estrogen receptor, Progesterone receptor and HER2/neu receptor status in Breast Cancer

Project description:Breast cancer is a heterogeneous disease encompassing a number of phenotypically diverse tumours. Expression levels of the estrogen, progesterone and HER2/neu receptors which characterise clinically distinct breast tumors have been shown to change during disease progression and in response to systemic therapies. Mi(cro)RNAs play critical roles in diverse biological processes and are aberrantly expressed in several human neoplasms including breast cancer, where they function as regulators of tumour behaviour and progression. The aims of this study were to identify miRNA signatures that accurately predict the oestrogen receptor (ER), progesterone receptor (PR) and HER2/neu receptor status of breast cancer patients to provide insight into the regulation of breast cancer phenotypes and progression.

2009-05-21 | GSE15885 | GEO

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

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