Abstract
The insulin receptor substrate-1 (IRS-1) and c-met, the receptor for the hepatocyte growth factor (HGF) co-immuno-precipitate from lysates treated with the respective antibodies. The interaction between IRS-1 and c-met requires a tyrosyl phosphorylated IRS-1 and results in reciprocal down-regulation. IRS-1 inhibits cell motility, while the activated c-met promotes it. These and other results suggest an explanation for reports in the literature indicating that c-met levels are high and IRS-1 levels are low in human cancer metastases.
(c) 2010 Wiley-Liss, Inc.
MeSH terms
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Animals
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Cell Line
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Cell Movement / physiology
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Down-Regulation*
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Extracellular Signal-Regulated MAP Kinases / metabolism
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Fibroblasts / cytology
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Fibroblasts / metabolism
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Hepatocyte Growth Factor / metabolism
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Humans
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Insulin Receptor Substrate Proteins / genetics
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Insulin Receptor Substrate Proteins / metabolism*
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Mice
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Phosphorylation
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Proto-Oncogene Proteins c-akt / metabolism
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Proto-Oncogene Proteins c-met / genetics
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Proto-Oncogene Proteins c-met / metabolism*
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Signal Transduction / physiology
Substances
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Insulin Receptor Substrate Proteins
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Hepatocyte Growth Factor
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Proto-Oncogene Proteins c-met
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Proto-Oncogene Proteins c-akt
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Extracellular Signal-Regulated MAP Kinases