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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: J Graham

PROVIDER: E-GEOD-31130 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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. 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.

2012-04-25 | E-GEOD-31129 | 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

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

The anti-proliferative effects of progestins in T47D breast cancer cells are tempered by progestin-induction of the ETS transcription factor Elf5.

Project description:Prolactin and progesterone act together to regulate mammary alveolar development, and both hormones have been implicated in breast cancer initiation and progression. Here we show that Elf5, a prolactin-induced ETS transcription factor that specifies the mammary secretory cell lineage, is also induced by progestins in breast cancer cells via a direct mechanism. To define the transcriptional response to progestin elicited via Elf5 we made an inducible Elf5 sh-RNA knock down model in T47D breast cancer cells and used it to prevent the progestin-induction of Elf5. Functional analysis of Affymetrix gene expression data using Gene Ontologies and Gene Set Enrichment Analysis showed enhancement of the progestin effects on cell cycle gene expression. Cell proliferation assays showed a more efficacious progestin-induced growth arrest when Elf5 was kept at baseline levels. These results showed that progestin-induction of Elf5 expression tempered the anti-proliferative effects of progestins in T47D cells, providing a further mechanistic link between prolactin and progestin in the regulation of mammary cell phenotype. We used Affymetrix expression arrays to determine to what extent Elf5 mediated the transcriptional effects of progestins in T47D cells. We transcript profiled our inducible Elf5 hold-down model using triplicate independent experiments under three conditions: (1) treatment with ethanol vehicle only (Baseline), (2) ORG2058 treatment for 4 days (Pg), and (3) Dox and ORG2058 treatment for 4 days, (Pg-Elf5) designed to prevent the progestin-induction of Elf5 expression.

2010-07-08 | E-GEOD-22363 | biostudies-arrayexpress

Gene expression profiling of T47D breast cancer cells following progestin administration in presence or absence of Telapristone

Project description:Analysis of the effect of progesterone blockade at the gene expression level. The hypothesis tested in the present study is that elapristone (CDB4124), an antiprogestin, will downregulate genes that are stimulated by R5020, a synthetic progestin, in the T47D breast cancer cell line. Total RNA obtained from T47 breast cancer cells grown for 24 hours in the presence of: 1. The sythetic progestin R5020 compared to vehicle control; 2. The antiprogestin Telapristone (CDB4124) compared to vehicle control; and 3. R5020 compared to R5020 ± Telapristone.

2015-05-15 | E-GEOD-67561 | 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

RNA-seq in two ER+ breast cancer cell lines with and without progestins

Project description:Exploring effect of progesterone/progestin treatment on gene expression Two cell lines, three conditions (Full Media with E2, E2+ Progesterone, Full Media + R5020 Progestin)

2015-05-22 | E-GEOD-68358 | biostudies-arrayexpress

ChIP-seq of ER, PR, p300 in two ER+ breast cancer cell lines treated with estrogen and with and without progestins

Project description:Exploring effect of progesterone/progestin treatment on ER and PR binding. Two cell lines, three conditions (Full Media with E2, E2+ Progesterone, Full Media + R5020 Progestin), three factors (ER, PR, p300), all with three replicates, each with a matched Input control.

2015-05-22 | E-GEOD-68355 | biostudies-arrayexpress

The anti-proliferative effects of progestins in T47D breast cancer cells are tempered by progestin-induction of the ETS transcription factor Elf5.

2010-06-17 | GSE22363 | GEO

Nucleosome driven transcription factor binding and gene regulation [microarray]

Project description:Elucidating the global function of a transcription factor implies the identification of its target genes and genomic binding sites. The role of chromatin in this context is unclear, but the dominant view is that factors bind preferentially to nucleosome-depleted regions, identified as DNaseI-hypersensitive sites (DHS). Here we show by chromatin-IP, MNase and DNaseI assays followed by deep sequencing that the progesterone receptor (PR) requires nucleosomes for optimal binding and function. In breast cancer cells treated with progestins we identified 25,000 PR binding sites (PRbs), the majority encompassing several copies of the hexanucleotide TGTYCY, highly abundant in the genome. We found that functional PRbs accumulate around progesterone-induced genes mainly in enhancers, are enriched in DHS but exhibit high nucleosome occupancy. Progestin stimulation results in remodeling of these nucleosomes with displacement of histones H1 and H2A/H2B dimers. Our results strongly suggest that nucleosomes are crucial for PR binding and hormonal gene regulation. Keywords: time course Whole genome expression microarrays were performed in T47D-MTVL cells stimulated 0, 1 and 6 hr with 10 nM of progestin R5020. 3 biological replicas were performed for T0 and 6 hr treatments and 4 for the one of 1hr.

2012-12-01 | E-GEOD-41502 | biostudies-arrayexpress

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