Focal adhesion kinase N-terminus in breast carcinoma cells induces rounding, detachment and apoptosis

Lucia Beviglia, Vita Golubovskaya, Li Hui Xu, Xi Hui Yang, Rolf J. Craven, William G. Cance

Research output: Contribution to journalArticlepeer-review

48 Scopus citations


Focal adhesion kinase (FAK) has a central role in adhesion-mediated cell signalling. The N-terminus of FAK is thought to function as a docking site for a number of proteins, including the Src-family tyrosine kinases. In the present study, we disrupted FAK signalling by expressing the N-terminal domain of FAK (FAK-NT) in human breast carcinoma cells, BT474 and MCF-7 lines, and non-malignant epithelial cells, MCF-10A line. Expression of FAK-NT led to rounding, detachment and apoptosis in human breast cancer cells. Apoptosis was accompanied by dephosphorylation of FAK Tyr397, degradation of the endogenous FAK protein and activation of caspase-3. Over-expression of FAK rescued FAK-NT-mediated cellular rounding. Expression of FAK-NT in non-malignant breast epithelial cells did not lead to rounding, loss of FAK phosphorylation or apoptosis. Thus FAK-NT contributes to cellular adhesion and survival pathways in breast cancer cells which are not required for survival in non-malignant breast epithelial cells.

Original languageEnglish
Pages (from-to)201-210
Number of pages10
JournalBiochemical Journal
Issue number1
StatePublished - Jul 1 2003


  • Apoptosis
  • Breast cancer cell
  • Caspase activation
  • Protein degradation

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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