Abstract
Coexpression of the human Met receptor and its ligand, hepatocyte growth factor/scatter factor (HGF/SF), in NIH 3T3 fibroblasts causes the cells to become tumorigenic in nude mice. The resultant tumors display lumen-like morphology, contain carcinoma-like focal areas with intercellular junctions resembling desmosomes, and coexpress epithelial (cytokeratin) and mesenchymal (vimentin) cytoskeletal markers. The tumor cells also display enhanced expression of desmosomal and tight-junction proteins. The apparent mesenchymal to epithelial conversion of the tumor cells mimics the conversion that occurs during embryonic kidney development, suggesting that Met-HGF/SF signaling plays a role in this process as well as in tumors that express both epithelial and mesenchymal markers.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3T3 Cells
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Animals
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Cell Transformation, Neoplastic*
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Desmosomes / ultrastructure
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Epithelial Cells
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Hepatocyte Growth Factor / metabolism
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Hepatocyte Growth Factor / pharmacology
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Keratins / biosynthesis
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Kidney / embryology
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Kidney / metabolism
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Mesoderm / cytology
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Mice
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Mice, Nude
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Neoplasms, Experimental / metabolism
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Neoplasms, Experimental / pathology*
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Proto-Oncogene Mas
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins / metabolism*
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Proto-Oncogene Proteins c-met
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Proto-Oncogenes*
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Receptor Protein-Tyrosine Kinases / genetics
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Receptor Protein-Tyrosine Kinases / metabolism*
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Signal Transduction
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Transfection
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Vimentin / biosynthesis
Substances
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MAS1 protein, human
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Proto-Oncogene Mas
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Proto-Oncogene Proteins
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Vimentin
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Hepatocyte Growth Factor
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Keratins
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Proto-Oncogene Proteins c-met
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Receptor Protein-Tyrosine Kinases