| First Author | Tavora B | Year | 2010 |
| Journal | EMBO Mol Med | Volume | 2 |
| Issue | 12 | Pages | 516-28 |
| PubMed ID | 21154724 | Mgi Jnum | J:226147 |
| Mgi Id | MGI:5695837 | Doi | 10.1002/emmm.201000106 |
| Citation | Tavora B, et al. (2010) Endothelial FAK is required for tumour angiogenesis. EMBO Mol Med 2(12):516-28 |
| abstractText | Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase that plays a fundamental role in integrin and growth factor mediated signalling and is an important player in cell migration and proliferation, processes vital for angiogenesis. However, the role of FAK in adult pathological angiogenesis is unknown. We have generated endothelial-specific tamoxifen-inducible FAK knockout mice by crossing FAK-floxed (FAKfl/fl) mice with the platelet derived growth factor b (Pdgfb)-iCreER mice. Tamoxifen-treatment of Pdgfb-iCreER;FAKfl/fl mice results in FAK deletion in adult endothelial cells (ECs) without any adverse effects. Importantly however, endothelial FAK-deletion in adult mice inhibited tumour growth and reduced tumour angiogenesis. Furthermore, in in vivo angiogenic assays FAK deletion impairs vascular endothelial growth factor (VEGF)-induced neovascularization. In addition, in vitro deletion of FAK in ECs resulted in reduced VEGF-stimulated Akt phosphorylation and correlating reduced cellular proliferation as well as increased cell death. Our data suggest that FAK is required for adult pathological angiogenesis and validates FAK as a possible target for anti-angiogenic therapies. |
