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Updated: Jun 14, 2026

Isolation and Culture Expansion of Tumor-specific Endothelial Cells
Published on: October 14, 2015
Endothelial-Rac1 is not required for tumor angiogenesis unless alphavbeta3-integrin is absent
Gabriela D'Amico1, Stephen D Robinson, Mitchel Germain
1Adhesion and Angiogenesis Laboratory, Institute of Cancer, Bart's and The London, Queen Mary's School of Medicine and Dentistry, London, United Kingdom. gabriela.damico@helsinki.fi
Abstract:
Endothelial cell migration is an essential aspect of tumor angiogenesis. Rac1 activity is needed for cell migration in vitro implying a requirement for this molecule in angiogenesis in vivo. However, a precise role for Rac1 in tumor angiogenesis has never been addressed. Here we show that depletion of endothelial Rac1 expression in adult mice, unexpectedly, has no effect on tumor growth or tumor angiogenesis. In addition, repression of Rac1 expression does not inhibit VEGF-mediated angiogenesis in vivo or ex vivo, nor does it affect chemotactic migratory responses to VEGF in 3-dimensions. In contrast, the requirement for Rac1 in tumor growth and angiogenesis becomes important when endothelial beta3-integrin levels are reduced or absent: the enhanced tumor growth, tumor angiogenesis and VEGF-mediated responses in beta3-null mice are all Rac1-dependent. These data indicate that in the presence of alphavbeta3-integrin Rac1 is not required for tumor angiogenesis.
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