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syndecan, cells, cancer, pubmed, breast, expression, ibc, notch, article, sum, google, scholar, cell, egfr, nonibc, control, signaling, data, skbr, cas, fig, patients, mrna, negative, inflammatory, tissues, csc, knockdown, central, triple, tumor, positive, growth, carcinoma, silencing, levels, formation, phenotype, correlation, stem, van, flow, compared, analysis, stat, size, sirna, res, pathways, significantly,

Topics {✒️}

t-test/mann-whitney u-test nuclear factor-kappab dna-binding il6/jak1/stat3 signaling blockade nf-kappab/p65 signaling pathway syndecan-1 modulates beta-integrin-dependent quantitative real-time pcr stabilizing tumour-initiating cells martin götte nuclear factor-kappab signature anti-human-notch-2-pe & apc stem/progenitor cell properties mann-whitney u-test nf-kappab collaboration potential microenvironmental biomarkers carcinogen-induced tumor development article download pdf van golen kl triple-negative breast cancer transmembrane c-terminal fragment population-based cancer registry nf-kappab activation lung metastasis formation mmtv-pymt mouse model map kinase-dependent process mouse anti-human syndecan-1 rnai-mediated syndecan-1 silencing patient-derived xenograft tumors cultrex-coated petri-dishes cultrex-coated petri dishes raybio cytokine array-c3 lung cancer model sirna-mediated syndecan-1 knockdown autocrine feedback loop e-cadherin-dependent mechanism large population-based study triple negative mda-mb-23 jak2/stat3 signaling pathway cytoplasmic c-terminal fragment hrp–conjugated secondary antibodies cancer stem cell downstream signaling p-akt il-6-mediated stat3 signaling syndecan-1-silenced cells displayed anti-human-cd24-pe gamma-secretase inhibitor treatment wnt-1-induced mammary tumorigenesis il-6/jak2/stat3 pathway inflammatory breast cancer sherif abdelaziz ibrahim anti-human-cd44-fitc

Questions {❓}

• Notch signaling as a therapeutic target for breast cancer treatment?

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         headline:Syndecan-1 is a novel molecular marker for triple negative inflammatory breast cancer and modulates the cancer stem cell phenotype via the IL-6/STAT3, Notch and EGFR signaling pathways
         description:Inflammatory breast cancer (IBC), a particularly aggressive form of breast cancer, is characterized by cancer stem cell (CSC) phenotype. Due to a lack of targeted therapies, the identification of molecular markers of IBC is of major importance. The heparan sulfate proteoglycan Syndecan-1 acts as a coreceptor for growth factors and chemokines, modulating inflammation, tumor progression, and cancer stemness, thus it may emerge as a molecular marker for IBC. We characterized expression of Syndecan-1 and the CSC marker CD44, Notch-1 & -3 and EGFR in carcinoma tissues of triple negative IBC (n = 13) and non-IBC (n = 17) patients using qPCR and immunohistochemistry. Impact of siRNA-mediated Syndecan-1 knockdown on the CSC phenotype of the human triple negative IBC cell line SUM-149 and HER-2-overexpressing non-IBC SKBR3 cells employing qPCR, flow cytometry, Western blotting, secretome profiling and Notch pharmacological inhibition experiments. Data were statistically analyzed using Student’s t-test/Mann-Whitney U-test or one-way ANOVA followed by Tukey’s multiple comparison tests. Our data indicate upregulation and a significant positive correlation of Syndecan-1 with CD44 protein, and Notch-1 & -3 and EGFR mRNA in IBC vs non-IBC. ALDH1 activity and the CD44(+)CD24(-/low) subset as readout of a CSC phenotype were reduced upon Syndecan-1 knockdown. Functionally, Syndecan-1 silencing significantly reduced 3D spheroid and colony formation. Intriguingly, qPCR results indicate downregulation of the IL-6, IL-8, CCL20, gp130 and EGFR mRNA upon Syndecan-1 suppression in both cell lines. Moreover, Syndecan-1 silencing significantly downregulated Notch-1, -3, -4 and Hey-1 in SUM-149 cells, and downregulated only Notch-3 and Gli-1 mRNA in SKBR3 cells. Secretome profiling unveiled reduced IL-6, IL-8, GRO-alpha and GRO a/b/g cytokines in conditioned media of Syndecan-1 knockdown SUM-149 cells compared to controls. The constitutively activated STAT3 and NFκB, and expression of gp130, Notch-1 & -2, and EGFR proteins were suppressed upon Syndecan-1 ablation. Mechanistically, gamma-secretase inhibition experiments suggested that Syndecan-1 may regulate the expression of IL-6, IL-8, gp130, Hey-1, EGFR and p-Akt via Notch signaling. Syndecan-1 acts as a novel tissue biomarker and a modulator of CSC phenotype of triple negative IBC via the IL-6/STAT3, Notch and EGFR signaling pathways, thus emerging as a promising therapeutic target for IBC.
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         dateModified:2017-03-07T00:00:00Z
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            Syndecan-1
            Proteoglycan
            Cancer stem cell
            IL-6/STAT3
            Notch
            EGFR
            Cancer Research
            Oncology
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      headline:Syndecan-1 is a novel molecular marker for triple negative inflammatory breast cancer and modulates the cancer stem cell phenotype via the IL-6/STAT3, Notch and EGFR signaling pathways
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      dateModified:2017-03-07T00:00:00Z
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         Inflammatory breast cancer
         Syndecan-1
         Proteoglycan
         Cancer stem cell
         IL-6/STAT3
         Notch
         EGFR
         Cancer Research
         Oncology
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      name:Department of Zoology, Faculty of Science, Cairo University, Giza, Egypt
      name:Department of Zoology, Faculty of Science, Cairo University, Giza, Egypt
      name:Department of Zoology, Faculty of Science, Cairo University, Giza, Egypt
      name:Department of Radiotherapy–Radiooncology, University Hospital Münster, Münster, Germany
      name:Department of General Surgery, Faculty of Medicine, Ain Shams University, Cairo, Egypt
      name:Department of Zoology, Faculty of Science, Cairo University, Giza, Egypt
      name:Department of Gynecology and Obstetrics, Münster University Hospital, Münster, Germany

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