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• W2781683247 abstract "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 down-regulated, 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." @default.
• W2781683247 created "2018-01-12" @default.
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• W2781683247 date "2018-01-02" @default.
• W2781683247 modified "2023-10-16" @default.
• W2781683247 title "SUMOylation Regulates Transcription by the Progesterone Receptor A Isoform in a Target Gene Selective Manner" @default.
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• W2781683247 doi "https://doi.org/10.3390/diseases6010005" @default.
• W2781683247 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5871951" @default.
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• W2781683247 hasPublicationYear "2018" @default.
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