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cells, expression, gene, breast, genes, pubmed, cancer, expressing, article, google, scholar, figure, cell, cas, receptor, data, sumodeficient, msx, analysis, target, additional, tumors, file, progesterone, relative, upregulated, transcriptional, prb, levels, central, receptors, treatment, protein, phosphorylation, measured, progestin, sumoylation, prs, human, promoter, recruitment, enhancer, growth, treated, tumor, inducible, fold, signature, transcription, chromatin,

Topics {✒️}

pgc-1alpha-responsive genes involved pires-neo3 expression vector cell-titer-glo bioluminescence assays adding cell-titer-glo substrate camp-response element-binding protein sumo-sensitive pr target-genes 'sumo-sensitive' pr-target genes enhancer-driven lineage-specific transcription pr-b-specific transcriptional action expressing sumo-deficient pr phospho-ser294 pr proteins pre-existing 'open' regions 'feed-forward' vicious cycle total-rna polymerase ii erbb2-positive breast cancers 5% dextran-coated charcoal-treated growth factor-driven pathways covington & suzanne aw fuqua sumo-deficient kr pr gene-copy-number datasets derived proline-directed protein kinases erbb/mapk signaling pathway pr-dependent transcription peaks tamoxifen-treated er-positive tumors promote distinct patterns differential hormone-dependent phosphorylation sumo-deficient pr molecules pr-null expressing cells wilcoxon-signed rank tests sumo-deficient k388r prs undergo rapid ligand-dependent erbb2-positive breast tumors phospho-pr gene signature v-ras-induced transformation cell growth/death rates epidermal growth factor pr-dependent gene signature tissue-specific gene expression article download pdf glucocorticoid receptor phospho-isoforms multiple nuclear receptors pr-dependent gene expression high progesterone-receptor levels dynamic post-translational events kaplan-meier survival analysis pr-mediated cellular proliferation ligand-activated transcription factors sybr green master-mix kaplan-meier survival curve progestin-treated cells expressing

Questions {❓}

• Halford SE, Marko JF: How do site-specific DNA-binding proteins find their targets?

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WebPage:
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         headline:Phosphorylated and sumoylation-deficient progesterone receptors drive proliferative gene signatures during breast cancer progression
         description:Progesterone receptors (PR) are emerging as important breast cancer drivers. Phosphorylation events common to breast cancer cells impact PR transcriptional activity, in part by direct phosphorylation. PR-B but not PR-A isoforms are phosphorylated on Ser294 by mitogen activated protein kinase (MAPK) and cyclin dependent kinase 2 (CDK2). Phospho-Ser294 PRs are resistant to ligand-dependent Lys388 SUMOylation (that is, a repressive modification). Antagonism of PR small ubiquitin-like modifier (SUMO)ylation by mitogenic protein kinases suggests a mechanism for derepression (that is, transcriptional activation) of target genes. As a broad range of PR protein expression is observed clinically, a PR gene signature would provide a valuable marker of PR contribution to early breast cancer progression. Global gene expression patterns were measured in T47D and MCF-7 breast cancer cells expressing either wild-type (SUMOylation-capable) or K388R (SUMOylation-deficient) PRs and subjected to pathway analysis. Gene sets were validated by RT-qPCR. Recruitment of coregulators and histone methylation levels were determined by chromatin immunoprecipitation. Changes in cell proliferation and survival were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays and western blotting. Finally, human breast tumor cohort datasets were probed to identify PR-associated gene signatures; metagene analysis was employed to define survival rates in patients whose tumors express a PR gene signature. 'SUMO-sensitive' PR target genes primarily include genes required for proliferative and pro-survival signaling. DeSUMOylated K388R receptors are preferentially recruited to enhancer regions of derepressed genes (that is, MSX2, RGS2, MAP1A, and PDK4) with the steroid receptor coactivator, CREB-(cAMP-response element-binding protein)-binding protein (CBP), and mixed lineage leukemia 2 (MLL2), a histone methyltransferase mediator of nucleosome remodeling. PR SUMOylation blocks these events, suggesting that SUMO modification of PR prevents interactions with mediators of early chromatin remodeling at 'closed' enhancer regions. SUMO-deficient (phospho-Ser294) PR gene signatures are significantly associated with human epidermal growth factor 2 (ERBB2)-positive luminal breast tumors and predictive of early metastasis and shortened survival. Treatment with antiprogestin or MEK inhibitor abrogated expression of SUMO-sensitive PR target-genes and inhibited proliferation in BT-474 (estrogen receptor (ER)+/PR+/ERBB2+) breast cancer cells. We conclude that reversible PR SUMOylation/deSUMOylation profoundly alters target gene selection in breast cancer cells. Phosphorylation-induced PR deSUMOylation favors a permissive chromatin environment via recruitment of CBP and MLL2. Patients whose ER+/PR+ tumors are driven by hyperactive (that is, derepressed) phospho-PRs may benefit from endocrine (antiestrogen) therapies that contain an antiprogestin.
         datePublished:2012-06-14T00:00:00Z
         dateModified:2012-06-14T00:00:00Z
         pageStart:1
         pageEnd:23
         license:http://creativecommons.org/licenses/by/2.0/
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            Progesterone Receptor
            T47D Cell
            Progesterone Receptor Expression
            MSX2
            Reverse Transcription Quantitative Polymerase Chain Reaction
            Cancer Research
            Oncology
            Surgical Oncology
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      headline:Phosphorylated and sumoylation-deficient progesterone receptors drive proliferative gene signatures during breast cancer progression
      description:Progesterone receptors (PR) are emerging as important breast cancer drivers. Phosphorylation events common to breast cancer cells impact PR transcriptional activity, in part by direct phosphorylation. PR-B but not PR-A isoforms are phosphorylated on Ser294 by mitogen activated protein kinase (MAPK) and cyclin dependent kinase 2 (CDK2). Phospho-Ser294 PRs are resistant to ligand-dependent Lys388 SUMOylation (that is, a repressive modification). Antagonism of PR small ubiquitin-like modifier (SUMO)ylation by mitogenic protein kinases suggests a mechanism for derepression (that is, transcriptional activation) of target genes. As a broad range of PR protein expression is observed clinically, a PR gene signature would provide a valuable marker of PR contribution to early breast cancer progression. Global gene expression patterns were measured in T47D and MCF-7 breast cancer cells expressing either wild-type (SUMOylation-capable) or K388R (SUMOylation-deficient) PRs and subjected to pathway analysis. Gene sets were validated by RT-qPCR. Recruitment of coregulators and histone methylation levels were determined by chromatin immunoprecipitation. Changes in cell proliferation and survival were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays and western blotting. Finally, human breast tumor cohort datasets were probed to identify PR-associated gene signatures; metagene analysis was employed to define survival rates in patients whose tumors express a PR gene signature. 'SUMO-sensitive' PR target genes primarily include genes required for proliferative and pro-survival signaling. DeSUMOylated K388R receptors are preferentially recruited to enhancer regions of derepressed genes (that is, MSX2, RGS2, MAP1A, and PDK4) with the steroid receptor coactivator, CREB-(cAMP-response element-binding protein)-binding protein (CBP), and mixed lineage leukemia 2 (MLL2), a histone methyltransferase mediator of nucleosome remodeling. PR SUMOylation blocks these events, suggesting that SUMO modification of PR prevents interactions with mediators of early chromatin remodeling at 'closed' enhancer regions. SUMO-deficient (phospho-Ser294) PR gene signatures are significantly associated with human epidermal growth factor 2 (ERBB2)-positive luminal breast tumors and predictive of early metastasis and shortened survival. Treatment with antiprogestin or MEK inhibitor abrogated expression of SUMO-sensitive PR target-genes and inhibited proliferation in BT-474 (estrogen receptor (ER)+/PR+/ERBB2+) breast cancer cells. We conclude that reversible PR SUMOylation/deSUMOylation profoundly alters target gene selection in breast cancer cells. Phosphorylation-induced PR deSUMOylation favors a permissive chromatin environment via recruitment of CBP and MLL2. Patients whose ER+/PR+ tumors are driven by hyperactive (that is, derepressed) phospho-PRs may benefit from endocrine (antiestrogen) therapies that contain an antiprogestin.
      datePublished:2012-06-14T00:00:00Z
      dateModified:2012-06-14T00:00:00Z
      pageStart:1
      pageEnd:23
      license:http://creativecommons.org/licenses/by/2.0/
      sameAs:https://doi.org/10.1186/bcr3211
      keywords:
         Progesterone Receptor
         T47D Cell
         Progesterone Receptor Expression
         MSX2
         Reverse Transcription Quantitative Polymerase Chain Reaction
         Cancer Research
         Oncology
         Surgical Oncology
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            address:
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               type:PostalAddress
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      name:Suzanne AW Fuqua
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            address:
               name:Department of Medicine, Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, USA
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               type:PostalAddress
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      email:[email protected]
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      name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
      name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA
      name:Biostatistics and Bioinformatics Core, Masonic Cancer Center, Minneapolis, USA
      name:Biostatistics and Bioinformatics Core, Masonic Cancer Center, Minneapolis, USA
      name:Department of Medicine, Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, USA
      name:Department of Medicine, Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, USA
      name:Departments of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, Minneapolis, USA

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