Reversion of the transformed phenotype of B16 mouse melanoma: involvement of an 83 kd cell surface glycoprotein in specific growth inhibition |
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| Authors: | I Wieland G Müller S Braun W Birchmeier |
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| Affiliation: | 1. Department of Immunology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA;2. Tumor Immunology and Immunotherapy, Advanced Centre for Treatment, Research and Education in Cancer (ACTREC), Tata Memorial Centre, Kharghar, Navi Mumbai 410210, India;3. Division of Cancer Biology, DBT-Institute of Life Sciences, Bhubaneswar 751023, India;4. Department of Integrated Immunobiology, Duke School of Medicine, Durham, NC 27710, USA;5. Duke Cancer Institute, Duke School of Medicine, Durham, NC 27710, USA;6. Analytic Microscopy Core, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA;7. Proteomics and Metabolomics Core, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA;8. Department of Medicine, Duke School of Medicine, Durham, NC 27710, USA;9. Department of Biomedical Engineering, Knight Cancer Institute, and OHSU Center for Spatial Systems Biomedicine (OCSSB), Oregon Health and Science University, Portland, OR 97239, USA;10. Department of Genitourinary Oncology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA;11. Department of Radiation Therapy, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA;12. Departments of Medicine and Microbiology and Immunology, Dartmouth Geisel School of Medicine, Hanover, NH 03755, USA;13. Department of Biostatistics and Bioinformatics, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA;1. The Stem Cell Program, Department of Medicine, Boston Children’s Hospital, Boston, MA 02115, United States;2. Division of Gastroenterology and Nutrition, Department of Medicine, Boston Children’s Hospital, Boston, MA 02115, United States;3. Harvard Stem Cell Institute, Cambridge, MA 02138, United States;4. Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, United States;1. Randall Division of Cell and Molecular Biophysics, King’s College London, London SE1 1UL, UK;2. Department of Mechanical Engineering, University College London, London WC2R 2LS, UK;3. Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK;4. Centre de Recherche, Institut Curie, Paris, UMR168, France;1. Department of Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA;1. Technische Universität Braunschweig, Institut für Pharmazeutische Technologie, Mendelssohnstr. 1, 38106 Braunschweig, Germany;2. Technische Universität Braunschweig, Institut für Festkörpermechanik, Langer Kamp 8, 38106 Braunschweig, Germany;3. Leibniz Universität Hannover, Institut für Mehrphasenprozesse, Callinstr. 36, 30167 Hannover, Germany;4. Technische Universität Braunschweig, Zentrum für Pharmaverfahrenstechnik, Franz-Liszt-Str. 35a, 38106 Braunschweig, Germany |
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| Abstract: | Treating B16 mouse melanoma cells with monoclonal antibody NORM-2 reduces cell growth in tissue culture, agar, and syngeneic mice. We show that the NORM-2 antibody recognizes an integral 83 kd glycoprotein that is mobile in the plane of the plasma membrane of B16 melanoma cells. Expression of the glycoprotein is reduced under conditions that inhibit B16 growth, such as low serum, high cell density, and addition of transforming growth factor-beta. The glycoprotein reappears during S phase, when growth-arrested cells are restimulated. The NORM-2 antigen appears to be involved in growth regulation of B16 melanoma cells both in vitro and in vivo. |
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