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cancer, breast, cells, pubmed, irs, article, prb, cas, fig, google, scholar, cell, receptor, expression, models, phosphopr, mcf, insulin, gene, data, central, target, tumoursphere, resistance, tamr, progesterone, genes, endocrine, signalling, tumours, tamoxifen, formation, expressing, nature, metastatic, treatment, usa, levels, primary, pdx, tumourspheres, igfrβ, growth, supplementary, receptors, lesions, activity, protein, previously, relative,

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nature portfolio privacy policy goat anti-rabbit igg-hrp breast cancer research goat anti-mouse igg-hrp sumo-deficient/phospho-mimic pr advertising phospho-pr-specific gene signatures dextran-coated charcoal-stripped fbs prognostic index nature 523 nature 540 nature target phospho-pr-specific signalling real-time quantitative pcr standard light/dark cycle mitogen-activated protein kinase reprints key er/pr-binding partner irs-1/phospho-pr target genes single-cell phospho-pr levels anti-rabbit ig mp-7401 er/pr/c-src complexes estrogen receptor-alpha regulates er-positive breast cancer er+ breast tumors svetlana targeting phospho-pr/irs-1 crosstalk robust phospho-pr staining anti-mouse ig mp-7402 er/ps294-pr/irs-1 complexes phospho-pr gene signature specific pathogen-free housing stress-sensing protein kinases ultra-low attachment plates ultra-low attachment dishes data linking phospho-pr metastasis nod/scid/iliirg−/− endocrine-resistant breast cancer igf1rβ/ir hybrid receptors plenti cmv-neo vector cyclin-dependent kinase 4/6 phospho-pr target genes er-nfĸb-driven stem 16-gene phospho-ser294 pr 1 ml phosphate-buffered saline phenol red-free imem author information authors pr-induced target genes advanced breast cancer er/pr target genes

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         description:Progesterone receptors (PR) are potent modifiers of endocrine responses. In aberrant signalling cancer contexts, phosphorylation events dramatically alter steroid hormone receptor action. The transcriptomes of primary tumours and metastases in mice harbouring ER+ breast cancer patient-derived xenografts (PDXs) were analysed following single-cell RNAseq. In vitro assays were employed to delineate mechanisms of endocrine resistance and stemness. A 16-gene phospho-Ser294 PR (p-PR) signature predicted poor outcome in ER+ breast cancer. Relative to primary PDX tumours, metastatic lesions expressed abundant p-PR and exhibited an activated PR gene programme with elevated expression of PGR and IRS-1. Breast cancer models of activated PR lost the expression of IGF1R and acquired insulin hypersensitivity with tamoxifen insensitivity. Activated p-PR+ breast cancer cells formed increased tumourspheres with enlarged ALDH+ and CD24−/CD44 populations. E2 induced PR/IRS-1 interaction and exchange of IGF1Rβ for IRS-1 in p-PR-containing transcriptional complexes. Inhibition of IRS-1 or IR and inducible IRS-1 knockdown reduced tumourspheres. Endocrine-resistant models of luminal B breast cancer induced p-PR in 3D cultures and required PR and IRS-1 for tumoursphere formation. Phospho-PR-B cooperates with IRS-1 to promote outgrowth of endocrine-resistant and stem-like breast cancer cells. Targeting phospho-PR/IRS-1 crosstalk may block the emergence of endocrine resistance.
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