Abstract
Most cancer deaths result from spread of the primary tumor to distant sites (metastasis). MET is an important protein for metastasis in multiple tumor types. Here we report on the ability of tea catechins to suppress MET activation in human colon cancer cells and propose a mechanism by which they might compete for the kinase domain of the MET protein.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Antineoplastic Agents / chemistry
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Antineoplastic Agents / pharmacology*
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Camellia sinensis*
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Catechin / chemistry
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Catechin / pharmacology*
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Cell Line, Tumor
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Colonic Neoplasms
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Drug Screening Assays, Antitumor
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Flavonoids / pharmacology*
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Gallic Acid / chemistry
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Humans
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Kinetics
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Models, Molecular*
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Phenols / pharmacology*
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Polyphenols
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Proto-Oncogene Proteins / antagonists & inhibitors*
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Proto-Oncogene Proteins / chemistry
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Proto-Oncogene Proteins c-met
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Receptors, Growth Factor / antagonists & inhibitors*
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Receptors, Growth Factor / chemistry
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Structure-Activity Relationship
Substances
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Antineoplastic Agents
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Flavonoids
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Phenols
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Polyphenols
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Proto-Oncogene Proteins
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Receptors, Growth Factor
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Gallic Acid
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Catechin
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MET protein, human
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Proto-Oncogene Proteins c-met