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Genome-wide mapping of ligand-dependent progesterone receptor chromatin interactions in human breast cell lines using PR ChIP-seq

ABSTRACT: The effects of progesterone are pleiotropic, resulting in diverse outcomes in a range of target tissues. Progesterone signalling is mediated through the nuclear progesterone receptor (PR) and to identify whether the cell specificity of the PR transcriptome arises from distinct patterns of genomic interaction of PR, we have mapped the genomic binding sites for PR in breast cancer cells and minimally transformed breast cells. PR binding was correlated with transcriptional outcome in both cell lines. Three replicate PR ChIP samples and two replicate input DNA control samples from T-47D breast cancer cells and two replicate PR ChIP samples and two replicate input DNA control samples from AB32 transformed normal breast cells.

ORGANISM(S): Homo sapiens

SUBMITTER: J Graham

PROVIDER: E-GEOD-31129 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Non-overlapping progesterone receptor cistromes contribute to cell-specific transcriptional outcomes in breast cells

Project description:This SuperSeries is composed of the following subset Series: GSE31127: Impact of FOXA1 over-expression on progestin signalling in transformed normal breast cells GSE31128: Progestin regulation of gene expression in breast cancer and minimally transformed breast cell lines GSE31129: Genome-wide mapping of ligand-dependent progesterone receptor chromatin interactions in human breast cell lines using PR ChIP-seq Refer to individual Series

2012-04-25 | E-GEOD-31130 | biostudies-arrayexpress

Progestin regulation of gene expression in breast cancer and minimally transformed breast cell lines

Project description:Time course of response to synthetic progestin ORG2058 in T-47D and ZR-75-1 breast cancer cell lines and in two PR positive clones of the MCF-10A cell line: AB9 and AB32. Transcriptional response to synthetic progestin, 10nM ORG2058, was compared between the four cell lines at three treatment times. T-47D breast cancer cells were treated in triplicate with 10nM ORG2058 or ethanol vehicle and harvested at 2, 6 and 24h after treatment for gene expression profiling

2012-04-25 | E-GEOD-31128 | biostudies-arrayexpress

Progesterone receptor ChIP-seq within the mouse mammary gland

Project description:Progesterone (P) acting through its cognate nuclear receptors (PRs) plays an essential role in driving pregnancy-associated branching morphogenesis of the mammary gland. However, the fundamental mechanisms, including global cistromic and acute genomic transcriptional responses that are required to elicit active branching morphogenesis in response to P, have not been elucidated. We used chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) to identify P-regulated genes that directly recruit PRs in the mouse mammary gland after acute P treatment. Two replicate PR ChIP samples and two replicate input DNA control samples from mouse mammary glands after mice are treated subcutaneously with 17?-Estradiol for 24 hours and then 17?-Estradiol plus Progesterone for 6 hours.

2013-08-27 | E-GEOD-42887 | biostudies-arrayexpress

Impact of FOXA1 over-expression on progestin signalling in transformed normal breast cells

Project description:Genome wide gene expression profiling of response to synthetic progestin ORG2058 in AB32 cells, a PR positive clone of the MCF-10A cell line, was determined after lentiviral transduction with an expression construct encoding human FOXA1. Cells were treated for 6h or 24h with 10nM ORG2058 or vehicle, 48h after transduction with the FOXA1 construct or empty vector control. Gene expression was measured in total RNA my Illumina whole genome gene expression array. Duplicate monolayer cultures of AB32 cells transduced 48h with pCDH-CMV-FOXA1-EF1-copGFP virus or negative control empty vector pCDH-CMV-mcs-EF1-copGFP virus were treated 6h or 24h with 10nM ORG2058 or 0.1% ethanol vehicle control. Cells were harvested for total RNA isolation and each sample was labelled and hybridized to a single Illumina human whole genome microarray, resulting in three replicate datasets for each of four conditions. Data were analysed separately and combined to give a mean signal intensity for each array probe.

2012-04-25 | E-GEOD-31127 | biostudies-arrayexpress

Genome-wide mapping of ligand-dependent progesterone receptor chromatin interactions in human breast cell lines using PR ChIP-seq

Project description:The effects of progesterone are pleiotropic, resulting in diverse outcomes in a range of target tissues. Progesterone signalling is mediated through the nuclear progesterone receptor (PR) and to identify whether the cell specificity of the PR transcriptome arises from distinct patterns of genomic interaction of PR, we have mapped the genomic binding sites for PR in breast cancer cells and minimally transformed breast cells. PR binding was correlated with transcriptional outcome in both cell lines.

2012-04-26 | GSE31129 | GEO

Selective suppression of endothelial cytokine production by progesterone receptor [RNA-seq]

Project description:Steroid hormones are well-recognized suppressors of the inflammatory response, however, their cell- and tissue-specific effects in the regulation of inflammation are far less understood, particularly for the sex-related steroids. To determine the contribution of progesterone in the endothelium, we have characterized and validated an in vitro culture system in which human umbilical vein endothelial cells constitutively express human progesterone receptor (PR). Using next generation RNA-sequencing, we identified a selective group of cytokines that are suppressed by progesterone both under physiological conditions and during pathological activation by lipopolysaccharide. In particular, IL-6, IL-8, CXCL2/3, and CXCL1 were found to be direct targets of PR, as determined by ChIP-sequencing. Regulation of these cytokines by progesterone was also confirmed by bead-based multiplex cytokine assays and quantitative PCR. These findings provide a novel role for PR in the direct regulation of cytokine levels secreted by the endothelium. They also suggest that progesterone-PR signaling in the endothelium directly impacts leukocyte trafficking in PR-expressing tissues Examination of PR target genes in human umbilical vein endothelial cells (HUVECs) using RNA-seq PR infected only (PR); PR infected followed by ligand treatment (PR+P); PR infected followed by 4h LPS treatment (PR+LPs_4h); PR infected followed by 8h LPS treatment (PR+LPs_8h); PR infected followed by 4h LPS and progesterone treatment (PR+LPS+P_4h); PR infected followed by 8h LPS and progesterone treatment (PR+LPS+P_8h)

2014-01-01 | E-GEOD-46502 | biostudies-arrayexpress

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [tumor samples RNA-seq]

Project description:Transcriptomic changes and estrogen and progesterone receptor binding in multiple ER+/PR+ models (eight ER+/PR+ patient tumors, various T47Ds, ZR75) and multiple ER+/PR-negative models (four ER+/PR- patient tuumors, PR-deficient T47D and MCF7 cells) treated with various hormone combinations. Results: In isolation, estrogen and progestin act as genomic agonists by regulating the expression of common target genes in similar directions, but at different levels. Similarly, in isolation, progestin is also a weak phenotypic agonist of estrogen action. However, in the presence of both hormones, progestin behaves as a phenotypic estrogen antagonist. PR remodels nucleosomes to noncompetitively redirect ER genomic binding to distal enhancers enriched for BRCA1 binding motifs and sites that link PR and ER/PR complexes. Importantly, when both hormones are present, progestin modulates estrogen action such that responsive transcriptomes, cellular processes and ER/PR recruitment to genomic sites correlate with those observed with PR alone, but not ER alone. Conclusions: Genomic Agonism and Phenotypic Antagonism between Estrogen and Progesterone Receptors in Breast Cancer. Individual and concerted actions of ER and PR highlight the prognostic and therapeutic value of PR in ER+/PR+ breast cancers. ER+/PR+ and ER+/PR-deficient model systems were deprived of steroids by culturing them in phenol red free RPMI 1640 media that is supplemented with 10% charcoal-stripped fetal bovine serum and 1% penicillin/streptomycin. Subsequently, these steroid-deprived models were treated with either vehicle, 10 nM estradiol, 10 nM progestin R5020 or 10 nM of both the hormones and genomics (ChIP-seq and RNA-seq) was performed. ChIP-seq was done after 45 minutes of hormone treatments. For cell models, RNA-seq was done after 12 hours of hormone treatments. Tumor explants were treated with either 24 or 48 hours.

2016-06-01 | E-GEOD-80365 | biostudies-arrayexpress

Physiological Vascular Permeability Requires Induction of Endothelial NR4A1 by Progesterone Receptor [RNA-Seq]

Project description:Vascular permeability is frequently associated with inflammation and it is triggered by chemokines and by a cohort of secreted permeability factors, such as VEGF. In contrast, here we showed that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and it is independent of VEGF. Both global and endothelial-specific deletion of PR block physiological vascular permeability in the uterus while misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of genome-wide transcriptional profile of endothelium and ChIP-sequencing revealed that PR induces a NR4A1 (Nur77/TR3) specific transcriptional program that broadly regulates vascular permeability in response to progesterone. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely and venule-specific regulation of vascular barrier function. Silencing NR4A1 blocks PR-mediated permeability responses indicating a direct link between PR and NR4A1. These results reveal a previously unknown function for progesterone receptor on endothelial cell biology with consequences to physiological vascular permeability and implications to the clinical use of progestins and anti-progestins on blood vessel integrity. Examination of PR target genes in human umbilical vein endothelial cells (HUVECs) using RNA-seq (PR infected only -PR only and PR infected followed by ligand treatment-PR+P)

2014-01-01 | E-GEOD-43788 | biostudies-arrayexpress

Phosphorylated and SUMO-deficient progesterone receptors drive a gene expression profile important for breast cancer progression (Affymetrix gene expression analysis)

Project description:Anlaysis of the differential gene expression between T47D cells expressing wild type (WT) progesterone receptor isoform B (PR) or SUMOylation-deficient PR molecules. Total RNA obtained from T47D breast cancer cells induced (with AP21967) to express either iWT PR-B or mutant PR-B (iK388R, SUMO-deficient), treated with or without synthetic PR ligand R5020 for 6 h. Each sample had 1 replicate.

2012-06-06 | E-GEOD-34147 | biostudies-arrayexpress

Physiological Vascular Permeability Requires Induction of Endothelial NR4A1 by Progesterone Receptor [ChIP-Seq]

Project description:Vascular permeability is frequently associated with inflammation and it is triggered by chemokines and by a cohort of secreted permeability factors, such as VEGF. In contrast, here we showed that the physiological vascular permeability that precedes implantation is directly controlled by progesterone receptor (PR) and it is independent of VEGF. Both global and endothelial-specific deletion of PR block physiological vascular permeability in the uterus while misexpression of PR in the endothelium of other organs results in ectopic vascular leakage. Integration of genome-wide transcriptional profile of endothelium and ChIP-sequencing revealed that PR induces a NR4A1 (Nur77/TR3) specific transcriptional program that broadly regulates vascular permeability in response to progesterone. This program triggers concurrent suppression of several junctional proteins and leads to an effective, timely and venule-specific regulation of vascular barrier function. Silencing NR4A1 blocks PR-mediated permeability responses indicating a direct link between PR and NR4A1. These results reveal a previously unknown function for progesterone receptor on endothelial cell biology with consequences to physiological vascular permeability and implications to the clinical use of progestins and anti-progestins on blood vessel integrity. Examination of PR binding sites in HUVEC cells using ChIP-seq (non-infected-negative control, PR infected followed by ligand treatment-PR+P or vehicle PR)

2014-01-01 | E-GEOD-43786 | biostudies-arrayexpress

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