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Keywords {🔍}

foxc, cancer, cells, pubmed, article, cell, nsclc, betacatenin, google, scholar, fig, cas, expression, lung, protein, knockdown, stem, properties, resistance, levels, central, cscs, overexpression, tumor, csclike, cisplatin, gefitinib, percentage, signaling, chen, forkhead, docetaxel, target, breast, wang, survival, yang, human, drug, oct, nanog, effects, binding, sox, abcg, analysis, box, luciferase, activity, nonsmall,

Topics {✒️}

shbeta-catenin-expressing plasmid hsh054811–4-lvru6gp foxc1-expressing plasmid cs-x0042-lv217–01 pc9/g-shfoxc1-lv-beta-catenin nci-h1299-foxc1-lv-shbeta-catenin wnt/beta-catenin signaling pathway a549-shfoxc1-lv-beta-catenin pc9-foxc1-lv-shbeta-catenin small-cell lung cancer wnt/beta-catenin pathway atp-binding cassette subfamily beta-catenin-expressing plasmid nci-h1299-lv-foxc1 cells cytotoxic anti-cancer agents expressing plasmid hsh005629–33-lvru6rlp pc9/g-lv-shfoxc1 hui chen & rong xu epithelial-mesenchymal transdifferentiation lv-shbeta-catenin lentivirus mutant beta-catenin promoters activating nf-kappab signaling beta-catenin knockdown decreased c-kit mediates chemoresistance beta-catenin knockdown enhanced nuclear beta-catenin protein nsclc wnt/beta-catenin beta-catenin promoter sequence lv-beta-catenin lentivirus beta-catenin overexpression rescued perform real-time pcr upregulate beta-catenin expression beta-catenin knockdown attenuated foxc1-expressing cell lines real-time pcr assays beta-catenin overexpression attenuated knockdown beta-catenin expression beta-catenin/tcf determines beta-catenin protein levels nci-h1299-lv-foxc1 promoting beta-catenin expression shbeta-catenin target sequence wnt signaling pathway stemness-related gene expression triple-negative breast cancer beta-catenin mediates vegf-notch signaling pathways a549-lv-shfoxc1 cells ultra low-attachment plates overcoming egfr-tki resistance target protein-bound dna full-length foxc1 cdna

Questions {❓}

• Can lung cancer stem cells be targeted for therapies?

Schema {🗺️}

WebPage:
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         headline:FOXC1 induces cancer stem cell-like properties through upregulation of beta-catenin in NSCLC
         description:Accumulating evidence suggests that cancer stem cells (CSCs) play a critical role in tumor initiation, progression and therapy, and recent studies have indicated that Forkhead box C1 (FOXC1) is strongly associated with CSCs. This study investigates the regulatory effects of FOXC1 on CSC-like properties in non-small cell lung cancer (NSCLC). We analyzed FOXC1 expression in NSCLC using the Cancer Genome Atlas (TCGA) database on UALCANC and performed survival analyses of NSCLC patients on Human Protein Atlas. CSC-like properties were analyzed based on CSC marker-positive cell population, self-renewal ability, stemness-related gene expression, tumorigenicity and drug resistance. The percentage of CD133+ cells was analyzed by flow cytometric analysis. Self-renewal ability was detected by sphere-formation analysis. Real-time PCR, western blotting and immunohistochemical staining were employed to detect mRNA and protein levels. Tumorigenicity was determined based on a xenograft formation assay, and effects of FOXC1 on drug resistance were assessed by cell viability and apoptosis assays. Luciferase reporter and chromatin immunoprecipitation (ChIP) assays were used to investigate the binding of FOXC1 to beta-catenin promoter. FOXC1 expression was found to be elevated in NSCLC tissues and negatively correlated with patient survival. FOXC1 knockdown reduced CD133+ cell percentage, suppressed self-renewal ability, decreased expression of stemness-related genes (Oct4, NANOG, SOX2 and ABCG2) and inhibited NSCLC cell tumorigenicity in vivo. Moreover, FOXC1 knockdown increased cisplatin and docetaxel sensitivity and reduced gefitinib resistance, whereas FOXC1 overexpression enhanced CSC-like properties. Luciferase reporter and ChIP assays showed beta-catenin to be a direct transcriptional target of FOXC1. Furthermore, overexpression of beta-catenin reversed the CSC-like property inhibition induced by FOXC1 knockdown, and knockdown of beta-catenin attenuated the CSC-like properties induced by FOXC1 overexpression. This study demonstrates that FOXC1 induces CSC-like properties in NSCLC by promoting beta-catenin expression. The findings indicate that FOXC1 is a potential molecular target for anti-CSC-based therapies in NSCLC.
         datePublished:2018-09-06T00:00:00Z
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            Cancer stem cell-like properties
            Beta-catenin
            NSCLC
            Cancer Research
            Immunology
            Apoptosis
            Oncology
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      headline:FOXC1 induces cancer stem cell-like properties through upregulation of beta-catenin in NSCLC
      description:Accumulating evidence suggests that cancer stem cells (CSCs) play a critical role in tumor initiation, progression and therapy, and recent studies have indicated that Forkhead box C1 (FOXC1) is strongly associated with CSCs. This study investigates the regulatory effects of FOXC1 on CSC-like properties in non-small cell lung cancer (NSCLC). We analyzed FOXC1 expression in NSCLC using the Cancer Genome Atlas (TCGA) database on UALCANC and performed survival analyses of NSCLC patients on Human Protein Atlas. CSC-like properties were analyzed based on CSC marker-positive cell population, self-renewal ability, stemness-related gene expression, tumorigenicity and drug resistance. The percentage of CD133+ cells was analyzed by flow cytometric analysis. Self-renewal ability was detected by sphere-formation analysis. Real-time PCR, western blotting and immunohistochemical staining were employed to detect mRNA and protein levels. Tumorigenicity was determined based on a xenograft formation assay, and effects of FOXC1 on drug resistance were assessed by cell viability and apoptosis assays. Luciferase reporter and chromatin immunoprecipitation (ChIP) assays were used to investigate the binding of FOXC1 to beta-catenin promoter. FOXC1 expression was found to be elevated in NSCLC tissues and negatively correlated with patient survival. FOXC1 knockdown reduced CD133+ cell percentage, suppressed self-renewal ability, decreased expression of stemness-related genes (Oct4, NANOG, SOX2 and ABCG2) and inhibited NSCLC cell tumorigenicity in vivo. Moreover, FOXC1 knockdown increased cisplatin and docetaxel sensitivity and reduced gefitinib resistance, whereas FOXC1 overexpression enhanced CSC-like properties. Luciferase reporter and ChIP assays showed beta-catenin to be a direct transcriptional target of FOXC1. Furthermore, overexpression of beta-catenin reversed the CSC-like property inhibition induced by FOXC1 knockdown, and knockdown of beta-catenin attenuated the CSC-like properties induced by FOXC1 overexpression. This study demonstrates that FOXC1 induces CSC-like properties in NSCLC by promoting beta-catenin expression. The findings indicate that FOXC1 is a potential molecular target for anti-CSC-based therapies in NSCLC.
      datePublished:2018-09-06T00:00:00Z
      dateModified:2018-09-06T00:00:00Z
      pageStart:1
      pageEnd:12
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      keywords:
         FOXC1
         Cancer stem cell-like properties
         Beta-catenin
         NSCLC
         Cancer Research
         Immunology
         Apoptosis
         Oncology
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      name:Rong Xu
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      name:Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
      name:Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
      name:Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
      name:Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
      name:The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China
      name:Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
      name:The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China

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