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Keywords {🔍}

cells, breast, cancer, cell, gfp, google, scholar, article, luminal, pubmed, cas, fig, tdkpgfp, expression, lines, human, treated, tumors, ptreated, stem, compared, vehicle, progesterone, treatment, hormone, etoh, pinduced, progestins, mcf, progenitor, receptor, promoter, mrna, vehicletreated, fractions, induction, immunofluorescence, population, mammary, normal, cancers, control, data, levels, tumor, basallike, number, measured, fold, relative,

Topics {✒️}

p4-induced ck5‒er+pr+ cells p4-induced ck5+er‒pr‒ cells fluorescence-activated cell sorting intratumoral ck5−er+pr+ cells surrounding ck5‒er+pr+ cells initial p4-induced transformation progestin-driven mammary cancer facs-isolated p4-treated ck5+ ck5-positive cell line renewing ck5+er−pr− subpopulation anova/tukey post test avoid anti-proliferative therapeutics high-content imaging apparatus progestin-inducible ck5+ cells e2 + p4-treated ck5+ population reducing proteasome-dependent proteolysis cyclin-dependent inhibitor p27 e2 + p4-treated ck5− fraction p4-treated gfp+/ck5+ cells p4-treated gfp−/ck5− cells ck5 promoter–reporter cloning p4-treated gfp+/ck5+ population p4-regulated micrornas facilitate progesterone-induced ck5+ cells breast tumor heterogeneity e2 + p4-treated mcf7k5pgfp cells p4-induced ck5 expression estrogen receptor positive paracrine fgf/tbx3 signaling er+pr+ cell lines e2 + p4-treated gfp+ compared p4-induced ck5+ cells p4-induced ck5 cells positive breast cancer progestin-induced ck5+ cells p4-induced ck5+ population treatment-induced ck5+ cells intermediate ck5+ck18+ cells identify small-molecule modulators vybrant dyecycle violet mouse-generated primary antibodies β-actin loading controls e2-dependent pr expression mammosphere/3d-matrigel culture luminal estrogen receptor 100 μl 10 mm d-luciferin retinoic acid receptors human progesterone receptors p4-treated ck5+ cells p4-treated ck5− cells

Questions {❓}

• Gusterson B (2009) Do ‘basal-like’ breast cancers really exist?

Schema {🗺️}

WebPage:
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         headline:Progesterone-Inducible Cytokeratin 5-Positive Cells in Luminal Breast Cancer Exhibit Progenitor Properties
         description:Progestins play a deleterious role in the onset of breast cancer, yet their influence on existing breast cancer and tumor progression is not well understood. In luminal estrogen receptor (ER)- and progesterone receptor (PR)-positive breast cancer, progestins induce a fraction of cells to express cytokeratin 5 (CK5), a marker of basal epithelial and progenitor cells in the normal breast. CK5+ cells lose expression of ER and PR and are relatively quiescent, increasing their resistance to endocrine and chemotherapy compared to intratumoral CK5−ER+PR+ cells. Characterization of live CK5+ cells has been hampered by a lack of means for their direct isolation. Here, we describe optical (GFP) and bioluminescent (luciferase) reporter models to quantitate and isolate CK5+ cells in luminal breast cancer cell lines utilizing the human KRT5 gene promoter and a viral vector approach. Using this system, we confirmed that the induction of GFP+/CK5+ cells is specific to progestins, is dependent on PR, can be blocked by antiprogestins, and does not occur with other steroid hormones. Progestin-induced, fluorescence-activated cell sorting-isolated CK5+ cells had lower ER and PR mRNA, were slower cycling, and were relatively more invasive and sphere forming than their CK5− counterparts in vitro. Repeated progestin treatment and selection of GFP+ cells enriched for a persistent population of CK5+ cells, suggesting that this transition can be semi-permanent. These data support that in PR+ breast cancers, progestins induce a subpopulation of CK5+ER−PR− cells with enhanced progenitor properties and have implications for treatment resistance and recurrence in luminal breast cancer.
         datePublished:2012-11-27T00:00:00Z
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            Progesterone Receptor
            T47D Cell
            Progesterone Receptor Expression
            Luminal Breast Cancer
            Oncology
            Cancer Research
            Surgical Oncology
            Molecular Medicine
            Radiotherapy
            Internal Medicine
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      headline:Progesterone-Inducible Cytokeratin 5-Positive Cells in Luminal Breast Cancer Exhibit Progenitor Properties
      description:Progestins play a deleterious role in the onset of breast cancer, yet their influence on existing breast cancer and tumor progression is not well understood. In luminal estrogen receptor (ER)- and progesterone receptor (PR)-positive breast cancer, progestins induce a fraction of cells to express cytokeratin 5 (CK5), a marker of basal epithelial and progenitor cells in the normal breast. CK5+ cells lose expression of ER and PR and are relatively quiescent, increasing their resistance to endocrine and chemotherapy compared to intratumoral CK5−ER+PR+ cells. Characterization of live CK5+ cells has been hampered by a lack of means for their direct isolation. Here, we describe optical (GFP) and bioluminescent (luciferase) reporter models to quantitate and isolate CK5+ cells in luminal breast cancer cell lines utilizing the human KRT5 gene promoter and a viral vector approach. Using this system, we confirmed that the induction of GFP+/CK5+ cells is specific to progestins, is dependent on PR, can be blocked by antiprogestins, and does not occur with other steroid hormones. Progestin-induced, fluorescence-activated cell sorting-isolated CK5+ cells had lower ER and PR mRNA, were slower cycling, and were relatively more invasive and sphere forming than their CK5− counterparts in vitro. Repeated progestin treatment and selection of GFP+ cells enriched for a persistent population of CK5+ cells, suggesting that this transition can be semi-permanent. These data support that in PR+ breast cancers, progestins induce a subpopulation of CK5+ER−PR− cells with enhanced progenitor properties and have implications for treatment resistance and recurrence in luminal breast cancer.
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         Progesterone Receptor
         T47D Cell
         Progesterone Receptor Expression
         Luminal Breast Cancer
         Oncology
         Cancer Research
         Surgical Oncology
         Molecular Medicine
         Radiotherapy
         Internal Medicine
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