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Keywords {🔍}

cells, nanog, oct, cell, stat, lon, expression, hcc, figure, pstat, stem, cancer, snail, emt, tumor, article, pubmed, metastasis, assay, activation, lctrol, invasion, google, scholar, protein, cas, coexpression, transition, signaling, significantly, overexpression, epithelialmesenchymal, genes, octnanog, results, vivo, cat, carcinoma, proliferation, pathway, found, showed, nucleus, control, knockdown, analysis, gene, transcription, hepatocellular, properties,

Topics {✒️}

wei-zhong wu & zheng-gang ren alexa fluor®488-labeled anti-nanog alexa fluor®568-labeled anti-nanog anti-phospho-stat3 try705 antibody underwent epithelial-mesenchymal transition promote epithelial-mesenchymal transition inducing epithelial-mesenchymal transition epithelial-mesenchymal transition change promotes epithelial-mesenchymal transition zinc-finger transcription factors epithelial-mesenchymal transition phenotype jak-stat3-snail signaling pathway impacts cell differentiation oct4/nanog-mediated stat3 activation putative stat3-binding sites dmem-f12 medium supplemented oct4 regulates p-stat3 zheng-gang ren epithelial-mesenchymal transition epithelial mesenchymal transition oct4/nanog-induced snail expression ankyrin-regulated multidrug efflux anti-p-stat3-y705 antibody quantitative real-time pcr real-time rt-pcr anti-nanog-mediated immunoprecipitates article download pdf cloning vector pgmlv-sc1 oct4/nanog modulates activation ultra-low-attachment plate lentiviral vector pgmlv-pa6 epithelial gene e-cadherin anti-nanog monoclonal antibody represses e-cadherin transcription oct4/nanog-promoted snail expression specific pathogen-free conditions stat3-specific transcriptional activation shrna-mediated stat3 knockdown protein a-sepharose beads open access license oct4/nanog-mediated emt 20 ng/ml human bfgf immunoprecipitate dna-protein complexes sphere-forming ability assay embryonic stem cell stat3-dependent snail activation emt-phenotypic cancer cells oct4/nanog/stat3 signaling oct4/nanog-induced emt attenuates invasion/metastatic ability

Schema {🗺️}

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         headline:Coexpression of gene Oct4 and Nanog initiates stem cell characteristics in hepatocellular carcinoma and promotes epithelial-mesenchymal transition through activation of Stat3/Snail signaling
         description:Oct4 and Nanog are key regulatory genes that maintain the pluripotency and self-renewal properties of embryonic stem cells. We previously reported that the two stemness markers were tightly associated with cancer progression and poor outcomes of hepatocellular carcinoma. In this study, we demonstrate that coexpression of Oct4/Nanog modulates activation of signal transducer and activator of transcription 3 (Stat3), an oncogenic transcription factor that is activated in many human malignancies including hepatocellular carcinoma (HCC), as well as the expression of Snail, a key regulator implicated in epithelial-mesenchymal transition and tumor metastasis. Oct4 and Nanog were ectopic expressed in MHCC97-L cell lines via lentiviral gene transfection. The stemness characteristics including self-renewal, proliferation, chemoresistance, and tumorigenicity were assessed. The effect of coexpression of Oct4 and Nanog on epithelial-mesenchymal transition change, and the underlying molecular signaling was investigated. Ectopic coexpression of Oct4 and Nanog empowered MHCC97-L cells with cancer stem cell (CSC) properties, including self-renewal, extensive proliferation, drug resistance, and high tumorigenic capacity. Significantly, Oct4 and Nanog encouraged epithelial-mesenchymal transition change contributing to tumor migration, invasion/metastasis in vitro and in vivo. Following molecular mechanism investigation indicated Oct4/Nanog-regulated epithelial-mesenchymal transition change through Stat3-dependent Snail activation. Moreover, silencing Stat3 abrogates Oct4/Nanog-mediated epithelial-mesenchymal transition (EMT) change and invasion/metastasis in HCC. We delineate Oct4 and Nanog initiate stem cell characteristics in hepatocellular carcinoma and promote epithelial-mesenchymal transition through activation of Stat3/Snail signaling. Our findings propose Stat3/Snail pathway as a novel therapeutic target for the treatment of progression and metastasis of HCC with CSC-like signatures and epithelial-mesenchymal transition phenotype.
         datePublished:2015-03-11T00:00:00Z
         dateModified:2015-03-11T00:00:00Z
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            Nanog
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            Epithelial-mesenchymal transition
            Oncology
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      headline:Coexpression of gene Oct4 and Nanog initiates stem cell characteristics in hepatocellular carcinoma and promotes epithelial-mesenchymal transition through activation of Stat3/Snail signaling
      description:Oct4 and Nanog are key regulatory genes that maintain the pluripotency and self-renewal properties of embryonic stem cells. We previously reported that the two stemness markers were tightly associated with cancer progression and poor outcomes of hepatocellular carcinoma. In this study, we demonstrate that coexpression of Oct4/Nanog modulates activation of signal transducer and activator of transcription 3 (Stat3), an oncogenic transcription factor that is activated in many human malignancies including hepatocellular carcinoma (HCC), as well as the expression of Snail, a key regulator implicated in epithelial-mesenchymal transition and tumor metastasis. Oct4 and Nanog were ectopic expressed in MHCC97-L cell lines via lentiviral gene transfection. The stemness characteristics including self-renewal, proliferation, chemoresistance, and tumorigenicity were assessed. The effect of coexpression of Oct4 and Nanog on epithelial-mesenchymal transition change, and the underlying molecular signaling was investigated. Ectopic coexpression of Oct4 and Nanog empowered MHCC97-L cells with cancer stem cell (CSC) properties, including self-renewal, extensive proliferation, drug resistance, and high tumorigenic capacity. Significantly, Oct4 and Nanog encouraged epithelial-mesenchymal transition change contributing to tumor migration, invasion/metastasis in vitro and in vivo. Following molecular mechanism investigation indicated Oct4/Nanog-regulated epithelial-mesenchymal transition change through Stat3-dependent Snail activation. Moreover, silencing Stat3 abrogates Oct4/Nanog-mediated epithelial-mesenchymal transition (EMT) change and invasion/metastasis in HCC. We delineate Oct4 and Nanog initiate stem cell characteristics in hepatocellular carcinoma and promote epithelial-mesenchymal transition through activation of Stat3/Snail signaling. Our findings propose Stat3/Snail pathway as a novel therapeutic target for the treatment of progression and metastasis of HCC with CSC-like signatures and epithelial-mesenchymal transition phenotype.
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      dateModified:2015-03-11T00:00:00Z
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         Hepatocellular carcinoma
         Oct4
         Nanog
         Stat3
         Epithelial-mesenchymal transition
         Oncology
         Hematology
         Cancer Research
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      name:Liver Cancer Institute, Zhong Shan Hospital and Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Fudan University, Shanghai, China
      name:Liver Cancer Institute, Zhong Shan Hospital and Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Fudan University, Shanghai, China
      name:Liver Cancer Institute, Zhong Shan Hospital and Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Fudan University, Shanghai, China
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