Constitutively activated stat3 induces tumorigenesis and enhances cell motility of prostate epithelial cells through integrin β6 Academic Article uri icon


MeSH Major

  • Cell Movement
  • Epithelial Cells
  • Integrin beta Chains
  • Prostatic Neoplasms
  • STAT3 Transcription Factor


  • The persistent activation of signal transducer and activator of transcription 3 (Stat3) is a common feature of prostate cancer. However, little is known about the Stat3 targets that may mediate prostate tumorigenesis. The introduction of an activating mutant form of Stat3 (Stat3-C) into immortalized prostate epithelial cells resulted in tumorigenesis. Stat3-C-expressing cells had decreased E-cadherin levels, increased numbers of lamellipodia and stress fibers, and enhanced migratory capacities compared to vector control-expressing cells, with a concomitant increase in the expression of integrin beta6 and its ligand, fibronectin (FN). Exogenously added FN increased cellular migration, with a concomitant loss of E-cadherin expression. The blockade of integrin alphavbeta6 in Stat3-C-expressing cells inhibited migration, increased E-cadherin levels, and reduced colony formation in soft agar. These results demonstrate the sufficiency of constitutively activated Stat3 in mediating prostate tumorigenesis and identify novel Stat3 targets that are involved in promoting cell migration and transformation.

publication date

  • June 2007



  • Academic Article



  • eng

PubMed Central ID

  • PMC1900039

Digital Object Identifier (DOI)

  • 10.1128/MCB.02404-06

PubMed ID

  • 17438134

Additional Document Info

start page

  • 4444

end page

  • 53


  • 27


  • 12