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Updated: Jun 20, 2026

Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics
08:11

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Published on: March 26, 2018

The role of focal adhesion kinase in tumor initiation and progression

Paolo P Provenzano1, Patricia J Keely

  • 1Laboratory of Molecular Biology and Departments of Pharmacology and Biomedical Engineering, University of Wisconsin, Madison, WI, USA. ppproven@fhcrc.org

Cell Adhesion & Migration
|August 20, 2009
PubMed

Insights

Focal adhesion kinase (FAK) is crucial for cancer cell invasion and metastasis. Blocking FAK and its related pathways could be a promising strategy for developing new anti-cancer therapies targeting metastasis.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that regulates cell signaling pathways involved in proliferation, survival, and migration.
  • FAK is overexpressed in multiple human cancers, suggesting a role in tumorigenesis, but its causal role in tumor initiation and progression has not been extensively studied in transgenic models.
  • Previous research has established FAK's influence on critical adhesion and growth factor signaling pathways relevant to cancer.

Purpose of the Study:

  • To investigate the causal role of FAK in human cancer initiation and progression using transgenic mouse models.
  • To determine the consequences of FAK ablation in carcinoma and its impact on malignant conversion and metastasis.

Main Methods:

  • Utilized tissue-specific FAK-knockout mouse models of human cancer.
  • Analyzed the effects of FAK ablation on epithelial cell transformation, malignant conversion, and metastasis.
  • Investigated downstream signaling pathways including Src, p130Cas, actin cytoskeleton dynamics, and Rho GTPase signaling.

Main Results:

  • Epithelial cells can transform without FAK, but they fail to undergo malignant conversion to invasive carcinoma.
  • FAK ablation significantly impairs metastasis.
  • Decreased Src and p130Cas activation, along with misregulated actin cytoskeleton dynamics and Rho GTPase signaling, were observed in the absence of FAK.

Conclusions:

  • FAK plays a critical role in promoting malignant conversion and metastasis in cancer.
  • The FAK-regulating/regulated signaling network represents a viable therapeutic target for inhibiting cancer metastasis.
  • Targeting FAK could offer a novel strategy for anti-metastasis cancer therapies.

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