Abstract
The p53 transcription factor, discovered in 1979 ( 1;2) , is well known as a potent suppressor of tumor development by inhibiting cell cycle progression, and promoting senescence or apoptosis, when the genome is compromised or under oncogenic stress ( 3) . Accumulating evidence has pointed to an alternative role of p53 in the curtailment of tumor progression and colonization of secondary sites by negatively regulating tumor cell metastasis ( 4;5) . Recently, we have found that p53 suppresses Src-induced formation of podosomes and associated invasive phenotypes in fibroblasts and vascular smooth muscle cells (VSMC) ( 6;7) . In this review, I will focus on some recent studies that have identified p53 as a suppressor of cell migration and invasion in general, and VSMC podosome formation and ECM degradation in particular.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Actins / genetics
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Actins / metabolism
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Animals
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Apoptosis
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Calmodulin-Binding Proteins / genetics
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Calmodulin-Binding Proteins / metabolism*
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Cell Communication
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Cell Movement
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Cortactin / genetics
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Cortactin / metabolism
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Cytoskeleton / physiology
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Extracellular Matrix / metabolism
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Extracellular Matrix / pathology
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Fibroblasts / cytology
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Fibroblasts / metabolism
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Gene Expression Regulation
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Genes, p53
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Genes, src
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Humans
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Mice
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Muscle, Smooth, Vascular / cytology
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Muscle, Smooth, Vascular / metabolism
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PTEN Phosphohydrolase / genetics
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PTEN Phosphohydrolase / metabolism
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Phosphorylation
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Rats
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Rosette Formation
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STAT3 Transcription Factor / genetics
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STAT3 Transcription Factor / metabolism
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Signal Transduction
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism*
Substances
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Actins
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Calmodulin-Binding Proteins
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Cortactin
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STAT3 Transcription Factor
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Tumor Suppressor Protein p53
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PTEN Phosphohydrolase