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

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

PROVIDER: PRJNA150063 | ENA |

REPOSITORIES: ENA

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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)

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 | GSE34147 | GEO

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

Project description:This SuperSeries is composed of the following subset Series: GSE34147: Phosphorylated and SUMO-deficient progesterone receptors drive a gene expression profile important for breast cancer progression (Affymetrix gene expression analysis) GSE34148: Phosphorylated and SUMO-deficient progesterone receptors drive a gene expression profile important for breast cancer progression (Illumina gene expression analysis) Refer to individual Series

2012-06-06 | E-GEOD-34149 | biostudies-arrayexpress

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

Project description: Not available

| S-EPMC3446358 | biostudies-literature

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

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

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

SUMOylation Regulates the Anti-Proliferative Gene Signature Programs of Glucocorticoid Receptor (HEK293)

Project description:In addition to the glucocorticoids, the glucocorticoid receptor (GR) is regulated by post-translational modifications, including SUMOylation. We have analyzed how SUMOylation influences the activity of endogenous GR target genes and the receptor chromatin binding by using isogenic HEK293 cells expressing wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR). Gene expression profiling revealed that both dexamethasone up- and down-regulated genes are affected by the GR sumoylation and that the affected genes are significantly associated with pathways of cellular proliferation and survival. The GR3KR-expressing cells proliferated more rapidly and their anti-proliferative response to dexamethasone was less pronounced than in the wtGR-expressing cells. ChIP-seq analyses indicated that the SUMOylation modulates the chromatin occupancy of GR on several loci associated with cellular growth in a fashion which parallels with their differential dexamethasone-regulated expression between the two cell lines. Moreover, genome-wide SUMO-2/3 marks, which were generally associated with active chromatin, showed markedly higher overlap with the wtGR cistrome than with the GR3KR cistrome. In sum, our results indicate that the SUMOylation does not simply repress the GR activity, but regulates the activity of the receptor in a target locus selective fashion, playing an important role in controlling the GR activity on genes influencing cell growth. Total RNA isolated from isogenic HEK293 cell lines stably expressing either wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR) treated with either vehicle (EtOH) or 100 nM of dexamethasone (dex) for 6h. All conditions are performed in triplicate

2013-11-05 | E-GEOD-48328 | biostudies-arrayexpress

SUMOylation Regulates the Anti-Proliferative Gene Signature Programs of Glucocorticoid Receptor (U2Os cell line)

Project description:In addition to the glucocorticoids, the glucocorticoid receptor (GR) is regulated by post-translational modifications, including SUMOylation. We have analyzed how SUMOylation influences the activity of endogenous GR target genes and the receptor chromatin binding by using isogenic HEK293 cells expressing wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR). Gene expression profiling revealed that both dexamethasone up- and down-regulated genes are affected by the GR sumoylation and that the affected genes are significantly associated with pathways of cellular proliferation and survival. The GR3KR-expressing cells proliferated more rapidly and their anti-proliferative response to dexamethasone was less pronounced than in the wtGR-expressing cells. ChIP-seq analyses indicated that the SUMOylation modulates the chromatin occupancy of GR on several loci associated with cellular growth in a fashion which parallels with their differential dexamethasone-regulated expression between the two cell lines. Moreover, genome-wide SUMO-2/3 marks, which were generally associated with active chromatin, showed markedly higher overlap with the wtGR cistrome than with the GR3KR cistrome. In sum, our results indicate that the SUMOylation does not simply repress the GR activity, but regulates the activity of the receptor in a target locus selective fashion, playing an important role in controlling the GR activity on genes influencing cell growth. Total RNA isolated from U2Os cell lines stably expressing either wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR) treated with either vehicle (EtOH) or 100 nM of dexamethasone (dex) for 6h.

2013-11-05 | E-GEOD-48330 | biostudies-arrayexpress

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