Abstract
Metastasis-associated protein 1 (MTA1) is highly upregulated in cancer cells with metastatic potential; however, the molecular mechanism by which MTA1 increases the metastatic potential of cancer cells is far from clear. We characterized the functional consequences of MTA1 overexpression on p53-induced apoptosis of cancer cells. MTA1 was associated with p53 in a co-immunoprecipitation assay. MTA1 also had deacetylation activity on p53 in human non-small cell lung cancer cells H1299 and human hepatoma cells SK-Hep1. MTA1 attenuated the transactivation and p21 induction by p53. Moreover, MTA1 expression decreased p53-mediated apoptosis. These results indicate that MTA1 inhibits p53-induced apoptosis by deacetylation of p53, which might be related to the increased metastatic potential of cancer cells with high MTA1 expression.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylation
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Apoptosis*
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Blotting, Western
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Carcinoma, Hepatocellular / metabolism
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Carcinoma, Hepatocellular / pathology
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Cells, Cultured
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Cyclin-Dependent Kinase Inhibitor p21 / metabolism
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Gene Expression Regulation, Neoplastic*
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Histone Deacetylases / pharmacology*
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Humans
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Immunoprecipitation
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Kidney / metabolism
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Kidney / pathology
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Liver Neoplasms / metabolism
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Liver Neoplasms / pathology
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Luciferases / metabolism
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Lung Neoplasms / metabolism
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Lung Neoplasms / pathology
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Repressor Proteins / pharmacology*
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Trans-Activators
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Transcription, Genetic
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism*
Substances
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Cyclin-Dependent Kinase Inhibitor p21
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MTA1 protein, human
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Repressor Proteins
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Trans-Activators
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Tumor Suppressor Protein p53
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Luciferases
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Histone Deacetylases