Abstract
Tumor progression is a multi-step process that requires a sequential selection of specific malignant phenotypes. Met activation may induce different phenotypes depending on tumor stage: inducing proliferation and angiogenesis in primary tumors, stimulating motility to form micrometastases, and regaining the proliferation phenotype to form overt metastases. To study how HGF/SF-induced proliferative phenotypes switch to the invasive phenotype is important for understanding the mechanism of tumor progression and will provide an attractive target for cancer intervention and therapy.
MeSH terms
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Adaptor Proteins, Signal Transducing / metabolism
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Animals
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Cell Proliferation
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Disease Progression*
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GRB2 Adaptor Protein
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Hepatocyte Growth Factor / metabolism*
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Humans
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Inositol Polyphosphate 5-Phosphatases
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Models, Biological
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Neoplasm Metastasis
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Neoplasms / metabolism
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Neoplasms / pathology*
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Neovascularization, Pathologic
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Phenotype
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Phosphoric Monoester Hydrolases / metabolism
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Proto-Oncogene Proteins / metabolism
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Proto-Oncogene Proteins c-cbl
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Proto-Oncogene Proteins c-met / metabolism*
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Signal Transduction*
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Ubiquitin-Protein Ligases / metabolism
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ras Proteins / metabolism
Substances
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Adaptor Proteins, Signal Transducing
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GRB2 Adaptor Protein
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GRB2 protein, human
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Proto-Oncogene Proteins
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Hepatocyte Growth Factor
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Proto-Oncogene Proteins c-cbl
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Ubiquitin-Protein Ligases
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Proto-Oncogene Proteins c-met
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Phosphoric Monoester Hydrolases
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Inositol Polyphosphate 5-Phosphatases
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ras Proteins