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Updated: Jun 6, 2026
10:15
Isolation and Culture Expansion of Tumor-specific Endothelial Cells
Published on: October 14, 2015
Endothelial FAK is required for tumour angiogenesis
Bernardo Tavora1, Silvia Batista, Louise E Reynolds
1Adhesion and Angiogenesis Laboratory, Centre of Tumour Biology, Institute of Cancer and Cancer Research UK Clinical Centre, Barts & The London, Queen Mary's School of Medicine & Dentistry, John Vane Science Centre, Charterhouse Square, London, UK.
EMBO Molecular Medicine
|December 15, 2010
Summary
Focal adhesion kinase (FAK) is crucial for new blood vessel growth. Inhibiting FAK in adult endothelial cells reduced tumor growth and blood vessel formation, suggesting FAK as a therapeutic target.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- Focal adhesion kinase (FAK) is a key signaling molecule in cell migration and proliferation.
- Its role in adult pathological angiogenesis remains unclear.
- Angiogenesis is vital for tumor growth and metastasis.
Purpose of the Study:
- To investigate the role of FAK in adult pathological angiogenesis.
- To determine if FAK is a viable target for anti-angiogenic therapies.
Main Methods:
- Generated endothelial-specific tamoxifen-inducible FAK knockout mice.
- Administered tamoxifen to induce FAK deletion in adult endothelial cells (ECs).
- Assessed tumor growth, angiogenesis, and in vitro EC behavior.
Main Results:
- Endothelial FAK deletion inhibited tumor growth and reduced tumor angiogenesis.
- FAK deletion impaired vascular endothelial growth factor (VEGF)-induced neovascularization in vivo.
- In vitro, FAK deletion reduced VEGF-stimulated Akt phosphorylation, proliferation, and increased cell death.
Conclusions:
- FAK is essential for adult pathological angiogenesis.
- Targeting FAK may be a promising strategy for anti-angiogenic therapies.
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