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Molecular Pathways: Endothelial Cell FAK-A Target for Cancer Treatment

Marina Roy-Luzarraga1, Kairbaan Hodivala-Dilke2

  • 1Adhesion and Angiogenesis Laboratory, Centre for Tumor Biology, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|June 5, 2016
PubMed

Insights

Focal adhesion kinase (FAK) in endothelial cells regulates chemotherapy response. Inhibiting FAK in these cells can sensitize tumors to DNA-damaging therapies, reducing tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Focal adhesion kinase (FAK, PTK2) is a nonreceptor protein tyrosine kinase crucial for signal transduction.
  • FAK is upregulated in advanced solid tumors, promoting progression and metastasis.
  • FAK inhibitors are under clinical investigation for cancer treatment.

Purpose of the Study:

  • To summarize the roles of endothelial cell FAK (EC-FAK) in cancer and development.
  • To review the current status of FAK-targeting anticancer strategies.
  • To highlight EC-FAK's role in regulating chemosensitivity.

Main Methods:

  • Review of existing literature on FAK in cancer and endothelial cells.
  • Analysis of FAK's role in tumor microenvironment and signal transduction.
  • Summary of clinical trial data for FAK inhibitors.

Main Results:

  • Endothelial cell FAK (EC-FAK) is identified as a key regulator of chemosensitivity.
  • Loss of EC-FAK dysregulates angiocrine signals, leading to tumor cell chemosensitization.
  • Reduced tumor growth is observed when EC-FAK is inhibited, sensitizing malignant cells to DNA-damaging therapies.

Conclusions:

  • EC-FAK plays a significant role in cancer progression and response to therapy.
  • Targeting EC-FAK presents a novel strategy to enhance chemosensitivity.
  • FAK inhibitors targeting endothelial cells may improve efficacy of DNA-damaging cancer therapies.

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