v-Src-mediated transformation suppresses the expression of focal adhesion protein vinexin

Cancer Lett. 2009 Jun 28;279(1):22-9. doi: 10.1016/j.canlet.2009.01.017. Epub 2009 Feb 12.

Abstract

Expression of focal adhesion protein vinexin is reported to be altered in several cancer tissues; however, the mechanism of expressional change in vinexin is not known. Here we report the suppression of vinexin expression according to cellular transformation by v-Src. We found that vinexin expression was down-regulated both at the mRNA level and at the post-transcriptional level in v-Src-transformed cells. Both mTOR and MEK/ERK signals were involved in the suppression. Inhibition of these pathways by pharmacological treatment partially restored both vinexin protein and mRNA expression. Moreover, re-expression of vinexin in v-Src-transformed cells suppressed cell migration. Taken together, these observations suggest that cellular transformation by v-Src suppressed vinexin expression and that down-regulation of vinexin may be associated with oncogenic transformation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carrier Proteins / metabolism
  • Cell Movement
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism*
  • Cell Transformation, Neoplastic / pathology
  • Cell Transformation, Viral / genetics*
  • Dose-Response Relationship, Drug
  • Down-Regulation
  • Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Focal Adhesions / drug effects
  • Focal Adhesions / metabolism*
  • Genes, src*
  • Mice
  • Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase Kinases / metabolism
  • Muscle Proteins / genetics
  • Muscle Proteins / metabolism*
  • NIH 3T3 Cells
  • Phosphotransferases (Alcohol Group Acceptor) / metabolism
  • Protein Kinase Inhibitors / pharmacology
  • RNA, Messenger / metabolism
  • TOR Serine-Threonine Kinases
  • Time Factors
  • Transfection

Substances

  • Carrier Proteins
  • Muscle Proteins
  • Protein Kinase Inhibitors
  • RNA, Messenger
  • Sorbs3 protein, mouse
  • Phosphotransferases (Alcohol Group Acceptor)
  • mTOR protein, mouse
  • TOR Serine-Threonine Kinases
  • Extracellular Signal-Regulated MAP Kinases
  • Mitogen-Activated Protein Kinase Kinases