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Mechanism of Telapristone acetate (TPA) on Progesterone receptor (PR) action in T47D breast cancer cells

ABSTRACT: Mechanism of Telapristone acetate (TPA) on Progesterone receptor (PR) action in T47D breast cancer cells

PROVIDER: PRJNA453376 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7060050.fastq.gz	Fastqsanger.gz
	SRR7060060.fastq.gz	Fastqsanger.gz
	SRR7060051.fastq.gz	Fastqsanger.gz
	SRR7060061.fastq.gz	Fastqsanger.gz
	SRR7060052.fastq.gz	Fastqsanger.gz

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Mechanism of Telapristone acetate (TPA) on Progesterone receptor (PR) action in T47D breast cancer cells

Project description:To obtain a global analysis of the effect of TPA on the Progesterone Receptor (PR) cistrome

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Project description:Immuno-precipitation followed by MS was performed using the RIME protocol in this study. Estrogen Receptor (ER) and Progestorone Receptor (PR) were targetted using antibodies. The experiments were performed in a quantitative manner using SILAC labelling. Cells grown in complete serum (estrogenic) conditions were compared against an cells in similar complete media, however supplemented with Progesterone (PG) or R5020 for 4 hours. Experiments were performed in MCF7 and T47D cell lines

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Phosphorylated and Sumoylation-Deficient Progesterone Receptors Drive Proliferative Gene Signatures During Breast Cancer Progression (Illumina 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.

2012-06-07 | GSE34148 | GEO

Phosphorylated and Sumoylation-Deficient Progesterone Receptors Drive Proliferative Gene Signatures During Breast Cancer Progression (Affymetrix gene expression analysis)

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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 that express either WT PR-B or mutant PR-B (K388R, SUMO-deficient), treated with or without synthetic PR ligand R5020 for 6 h.

2012-06-06 | E-GEOD-34148 | 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.

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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.

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CHD8 controls progestin-dependent gene expression in T47D cells

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Project description:CHD8 is an ATPase of the SNF2 family involved in ATP-dependent nucleosome remodeling. Here we report data of the occupancy of CHD8 by ChIP-seq in human breast carcinoma T47D cells under different growing conditions. We show that under normal proliferation conditions CHD8 is mostly associated with promoters. Then, cells were subjected to 48 h or serum starvation followed by stimulation with the progesterone receptor (PR) agonist R5020 or with vehicle (ethanol), for 5 and 45 minutes. R5020 induced the fast association of CHD8 with a number of intergenic or intronic regions. We found that these regions were enriched in PR binding sites. Furthermore, they were enriched in H3K4me1 and P300, typical markers of enhancers. Therefore, our data indicate that in the presence of the PR agonist CHD8 is recruited to a number of PR enhancers. In additional experiments we demonstrated that CHD8 is required for activation of PR enhancers and for transcriptional regulation of progesterone-dependent genes.

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