CD44S-hyaluronan interactions protect cells resulting from EMT against anoikis |
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| Institution: | 1. AP-HP, Urgences, Samu 93, Hôpital Avicenne, Université Paris 13, Bobigny, France;2. AP-HP, Urgences, Centre de référence sur les angiœdèmes à kinines (CRéAk), Hôpital Louis Mourier, Université Paris 7, Colombes, France;3. AP-HP, Médecine Interne, DHUi2B, Centre de Référence associé sur les angiœdèmes à kinines (CRéAk), Hôpital Saint-Antoine, Université Paris 6, Paris, France;1. Department of Pathology, the Sol Goldman Pancreatic Cancer Research Center, the Johns Hopkins University School of Medicine, Baltimore, MD 21231;2. Department of Oncology, the Sol Goldman Pancreatic Cancer Research Center, the Johns Hopkins University School of Medicine, Baltimore, Maryland;3. Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York;3. Matrix Biology Program, Benaroya Research Institute at Virginia Mason, Seattle, Washington 98101;4. Department of Pathology, University of Washington, Seattle, Washington 98195;5. Department of Pathology, Stanford University School of Medicine, Stanford, California 94305;6. James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, St. Paul''s Hospital, Room 166, 1081 Burrard Street, Vancouver, British Columbia V6Z 1Y6, Canada;1. Physicochimie Curie (Institut Curie/Centre National de la Recherche Scientifique-UMR168/Université Pierre et Marie Curie), Institut Curie, Centre de Recherche, Paris, France;2. Matière et Système Complexes (Université Paris-Diderot/Centre National de la Recherche Scientifique-UMR 7057), Paris, France;3. Institut Curie/Centre National de la Recherche Scientifique-UMR144 /Université Pierre et Marie Curie, Institut Curie, Centre de Recherche, Paris, France |
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| Abstract: | The detachment of normal epithelial cells from matrix triggers an apoptotic response known as anoikis, during homeostatic turnover. Metastatic tumor cells evade anoikis, by mechanisms that are only partly characterized. In particular, the epithelial–mesenchymal transition (EMT) in a subset of invasive tumor cells confers anoikis-resistance. In some cases, EMT up-regulates the cancer stem cell marker CD44S and the enzyme hyaluronic acid synthase-2 (HAS2). CD44S is the major receptor for hyaluronan in the extracellular matrix. Herein, we demonstrate that CD44S, unlike the CD44E isoform expressed in normal epithelial cells, contributes to the protection against anoikis. This protection requires the interaction of CD44S with hyaluronan (HA). CD44S–HA interaction is proposed to play an important role in tumor metastasis through enhanced cell survival under detached conditions. |
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