Abstract:
:Genetic ablation of endothelial focal adhesion kinase (FAK) can inhibit pathological angiogenesis, suggesting that loss of endothelial FAK is sufficient to reduce neovascularization. Here we show that reduced stromal FAK expression in FAK-heterozygous mice unexpectedly enhances both B16F0 and CMT19T tumour growth and angiogenesis. We further demonstrate that cell proliferation and microvessel sprouting, but not migration, are increased in serum-stimulated FAK-heterozygous endothelial cells. FAK-heterozygous endothelial cells display an imbalance in FAK phosphorylation at pY397 and pY861 without changes in Pyk2 or Erk1/2 activity. By contrast, serum-stimulated phosphorylation of Akt is enhanced in FAK-heterozygous endothelial cells and these cells are more sensitive to Akt inhibition. Additionally, low doses of a pharmacological FAK inhibitor, although too low to affect FAK autophosphorylation in vitro, can enhance angiogenesis ex vivo and tumour growth in vivo. Our results highlight a potential novel role for FAK as a nonlinear, dose-dependent regulator of angiogenesis where heterozygous levels of FAK enhance angiogenesis.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Kostourou V,Lechertier T,Reynolds LE,Lees DM,Baker M,Jones DT,Tavora B,Ramjaun AR,Birdsey GM,Robinson SD,Parsons M,Randi AM,Hart IR,Hodivala-Dilke Kdoi
10.1038/ncomms3020subject
Has Abstractpub_date
2013-01-01 00:00:00pages
2020issn
2041-1723pii
ncomms3020journal_volume
4pub_type
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