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

ABSTRACT: Anlaysis of the differential gene expression between T47D cells expressing wild type (WT) progesterone receptor isoform B (PR) or SUMOylation-deficient PR molecules.

ORGANISM(S): Homo sapiens

PROVIDER: GSE34147 | GEO | 2012/06/07

SECONDARY ACCESSION(S): PRJNA156475

REPOSITORIES: GEO

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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 SUMO-deficient progesterone receptors drive a gene expression profile important for 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. 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.

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

SUMOylation Regulates Transcription by the Progesterone Receptor A Isoform in a Target Gene Selective Manner

Project description:Luminal breast cancers express estrogen (ER) and progesterone (PR) receptors, and respond to endocrine therapies. However, some ER+PR+ tumors display intrinsic or acquired resistance, possibly related to PR. Two PR isoforms, PR-A and PR-B, regulate distinct gene subsets that may differentially influence tumor fate. A high PR-A:PR-B ratio is associated with poor prognosis and tamoxifen resistance. We speculate that excessive PR-A marks tumors that will relapse early. Here we address mechanisms by which PR-A regulate transcription, focusing on SUMOylation. We use receptor mutants and synthetic promoter/reporters to show that SUMOylation deficiency or the deSUMOylase SENP1 enhance transcription by PR-A, independent of the receptors’ dimerization interface or DNA binding domain. De-SUMOylation exposes the agonist properties of the antiprogestin RU486. Thus, on synthetic promoters, SUMOylation functions as an independent brake on transcription by PR-A. What about PR-A SUMOylation of endogenous human breast cancer genes? To study these, we used gene expression profiling. Surprisingly, PR-A SUMOylation influences progestin target genes differentially, with some upregulated, others downregulated, and others unaffected. Hormone-independent gene regulation is also PR-A SUMOylation dependent. Several SUMOylated genes were analyzed in clinical breast cancer database. In sum, we show that SUMOylation does not simply repress PR-A. Rather, it regulates PR-A activity in a target selective manner including genes associated with poor prognosis, shortened survival, and metastasis.

2018-02-02 | GSE108607 | GEO

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

Project description:Phosphorylated and Sumoylation-Deficient Progesterone Receptors Drive Proliferative Gene Signatures During Breast Cancer Progression

| PRJNA150063 | ENA

Phosphorylated and sumoylation-deficient progesterone receptors drive proliferative gene signatures during breast cancer progression.

Project description: Not available

| S-EPMC3446358 | biostudies-literature

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer. [ChIP-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.

2016-06-01 | GSE80367 | GEO

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

2016-06-01 | GSE80366 | GEO

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

2016-06-01 | GSE80365 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-06-07 | GSE34149 | GEO