p53 regulation of podosome formation and cellular invasion in vascular smooth muscle cells

Cell Adh Migr. 2011 Mar-Apr;5(2):144-9. doi: 10.4161/cam.5.2.14375. Epub 2011 Mar 1.

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

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Actins / genetics
  • Actins / metabolism
  • Animals
  • Apoptosis
  • Calmodulin-Binding Proteins / genetics
  • Calmodulin-Binding Proteins / metabolism*
  • Cell Communication
  • Cell Movement
  • Cortactin / genetics
  • Cortactin / metabolism
  • Cytoskeleton / physiology
  • Extracellular Matrix / metabolism
  • Extracellular Matrix / pathology
  • Fibroblasts / cytology
  • Fibroblasts / metabolism
  • Gene Expression Regulation
  • Genes, p53
  • Genes, src
  • Humans
  • Mice
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / metabolism
  • PTEN Phosphohydrolase / genetics
  • PTEN Phosphohydrolase / metabolism
  • Phosphorylation
  • Rats
  • Rosette Formation
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Actins
  • Calmodulin-Binding Proteins
  • Cortactin
  • STAT3 Transcription Factor
  • Tumor Suppressor Protein p53
  • PTEN Phosphohydrolase