Focal adhesion kinase is required for bombesin-induced prostate cancer cell motility

Mol Cell Endocrinol. 2005 May 12;235(1-2):51-61. doi: 10.1016/j.mce.2004.06.014. Epub 2005 Mar 19.


Clinical evidence links neuroendocrine differentiation (NED) to prostate cancer progression. In the prostate carcinoma PC-3 cell model, the action of the gastrin releasing peptide (GRP) analog, bombesin (BN), on the activation of focal adhesion kinase (FAK) and invasiveness suggests that this kinase might favor metastasis. Given that components of the FAK signalling pathway are also up regulated in prostate cancer, the aim of the present investigation was to test if FAK function is required for BN-induced motility in PC-3 cells. In wound assays designed to investigate the fate of FAK in cells undergoing BN-induced motility, it was observed that BN treatment resulted in relocalization of FAK in focal contacts concomitantly with its tyrosine phosphorylation on residue 397 (FAK [pY(397)]) and with the formation of actin lamellipodia. Moreover, BN-induced cell motility was significantly reduced in the presence of FAK inhibitors (either anti-FAK [pY(397)] antibody or FRNK, the FAK-related non-kinase). Altogether, these observations point towards a critical role for FAK in the action of BN on PC-3 cell motility.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bombesin / pharmacology*
  • Cell Line, Tumor
  • Cell Movement / drug effects*
  • Focal Adhesion Kinase 1
  • Focal Adhesion Protein-Tyrosine Kinases
  • Humans
  • Male
  • Neoplasm Invasiveness
  • Prostatic Neoplasms / pathology*
  • Protein-Tyrosine Kinases
  • Pseudopodia / drug effects


  • Protein-Tyrosine Kinases
  • Focal Adhesion Kinase 1
  • Focal Adhesion Protein-Tyrosine Kinases
  • PTK2 protein, human
  • Bombesin