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migration are defining characteristics of metastatic cancer cells. Recent studies have documented that cell invasion during tumor progression may be critically dependent on the acquisition of epithelial–mesenchymal transition (EMT) features. EMT is a complex
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Departments of Urology, Anatomic Pathology, Department of Urology, Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, 3‐1‐1 Maidashi, Higashi‐ku, Fukuoka 812‐8582, Japan
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A Gleave ME 2012a Clusterin mediates TGF-β-induced epithelial-mesenchymal transition and metastasis via Twist1 in prostate cancer cells . Cancer Research 72 5261 – 5272 . ( doi:10.1158/0008-5472.CAN-12-0254 ). Shiota M Song Y Takeuchi
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kallikreins, implicated in prostate cancer ( Borgono & Diamandis 2004 , Clements et al. 2004 ). Epithelial-mesenchymal transition (EMT) is a crucial event in the progression of cancer to an invasive phenotype. The perturbation of E-cadherin and
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marker ( Fig. 6D ). The knockdown of the IR promoted a reversal of the epithelial–mesenchymal transition by repressing mesenchymal markers and re-expressing epithelial markers in the LCC6 IRKD tumors. Figure 5 EMT and angiogenesis in Ctrl and IRKD
Department of Pathology, Red Temática de Investigación Cooperativa en Cáncer (RETICC, Department of Pathology, Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocio/CSIC/Universidad de Sevilla, Avenida Manuel Siurot S/N, 41013 Seville, Spain
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coactivators TAZ and YAP, both of which contribute to epithelial–mesenchymal transition (EMT)-mediated cancer progression. A bidirectional relationship between YAP/TAZ and EMT, wherein a loss of cell polarity and cell–cell junctions induces the activation of
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the expression of FIBRONECTIN ( Fig. 6A , B and C ). As N-CADHERIN, VIM, FIBRONECTIN and E-CADHERIN are the key markers of epithelial–mesenchymal transition (EMT), these data show that SOX30 probably regulates the EMT process. Figure 6 SOX30
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Department of Development and Regeneration, Department of Hand Surgery, Zhejiang Provincial Key Laboratory of Ophthalmology, Eye Center of the 2nd Affiliated Hospital, Department of Imaging and Pathology, CITNOBA (National Research Council of Argentina), Laboratory of Pituitary Regulation, Unit Head and Neck Oncology, Research Group Experimental Oto‐Rhino‐Laryngology, Unit Clinical and Experimental Endocrinology, Research Group Experimental Neurosurgery and Neuroanatomy, Cluster Stem Cell Biology and Embryology, Research Unit of Stem Cell Research, KU Leuven (University of Leuven), Campus Gasthuisberg O&N4, Herestraat 49, B-3000 Leuven, Belgium
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Department of Development and Regeneration, Department of Hand Surgery, Zhejiang Provincial Key Laboratory of Ophthalmology, Eye Center of the 2nd Affiliated Hospital, Department of Imaging and Pathology, CITNOBA (National Research Council of Argentina), Laboratory of Pituitary Regulation, Unit Head and Neck Oncology, Research Group Experimental Oto‐Rhino‐Laryngology, Unit Clinical and Experimental Endocrinology, Research Group Experimental Neurosurgery and Neuroanatomy, Cluster Stem Cell Biology and Embryology, Research Unit of Stem Cell Research, KU Leuven (University of Leuven), Campus Gasthuisberg O&N4, Herestraat 49, B-3000 Leuven, Belgium
Department of Development and Regeneration, Department of Hand Surgery, Zhejiang Provincial Key Laboratory of Ophthalmology, Eye Center of the 2nd Affiliated Hospital, Department of Imaging and Pathology, CITNOBA (National Research Council of Argentina), Laboratory of Pituitary Regulation, Unit Head and Neck Oncology, Research Group Experimental Oto‐Rhino‐Laryngology, Unit Clinical and Experimental Endocrinology, Research Group Experimental Neurosurgery and Neuroanatomy, Cluster Stem Cell Biology and Embryology, Research Unit of Stem Cell Research, KU Leuven (University of Leuven), Campus Gasthuisberg O&N4, Herestraat 49, B-3000 Leuven, Belgium
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regrowing the (heterogeneous) tumor ( Vankelecom & Gremeaux 2010 , Clevers 2011 , Vankelecom 2012 , Vankelecom & Chen 2014 ). Recently, CSCs have been reported to display characteristics of epithelial–mesenchymal transition (EMT), which may drive these
Department of Medicine III, University Hospital Carl Gustav Carus, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse, Dresden, Germany
Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
German Center for Diabetes Research (DZD), München-Neuherberg, Germany
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Institute of Physiology, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse, Dresden, Germany
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Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Madrid, Spain
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Department of Endocrinology, Diabetology and Clinical Nutrition, UniviersitätsSpital Zürich, Zurich, Switzerland
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Faculty of Chemistry and Food Chemistry, School of Science, Technische Universität Dresden, Mommsenstrasse, Dresden, Germany
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Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Madrid, Spain
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German Consortium for Translational Cancer Research (DKTK), partner site Essen/Düsseldorf, Düsseldorf, Germany
Department of Pediatric Oncology, Hematology, and Clinical Immunology, Medical Faculty, University Hospital Düsseldorf, Düsseldorf, Germany
Department of Neuropathology, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany
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Department of Medicine III, University Hospital Carl Gustav Carus, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, Fetscherstrasse, Dresden, Germany
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the acquisition of a motile and invasive tumor cell phenotype (epithelial–mesenchymal transition, EMT). Our data indicated for the first time that HIF2α increases motility and migration capacity of pheochromocytoma cells by inducing EMT (A). Moreover
Department of Pathology & Molecular Medicine, Queen’s University, Kingston, Ontario, Canada
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Department of Pathology & Molecular Medicine, Queen’s University, Kingston, Ontario, Canada
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Department of Pathology & Molecular Medicine, Queen’s University, Kingston, Ontario, Canada
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Department of Pathology & Molecular Medicine, Queen’s University, Kingston, Ontario, Canada
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Department of Medical Genetics, University of British Columbia, British Columbia Cancer Research Centre, Vancouver, British Columbia, Canada
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Department of Pathology & Molecular Medicine, Queen’s University, Kingston, Ontario, Canada
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JK Rocchi S Mallavialle A Galibert MD Khammari A 2012 The epithelial-mesenchymal transition (EMT) regulatory factor SLUG (SNAI2) is a downstream target of SPARC and AKT in promoting melanoma cell invasion . PLoS ONE 7 e40378
Lab of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium
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Université Paris-Saclay, INRAE, AgroParisTech, GABI, Jouy-en-Josas, Ile-de-France, France
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Epithelial-mesenchymal transition (EMT) signature is inversely associated with T-cell infiltration in non-small cell lung cancer (NSCLC) . Scientific Reports 8 2918. ( https://doi.org/10.1038/s41598-018-21061-1 ) Cordina-Duverger E Menegaux F Popa