Another exciting paper published in Communocations Biology from our client at Department of Molecular and Cellular Oncology, University of Texas MD Anderson Cancer Center. In their paper Song Yi Ko and co-authors have demonstrated that Cancer-derived small extracellular vesicles promote angiogenesis by heparin-bound, bevacizumab-insensitive VEGF. Increasing evidence indicates that stromal reprogramming in cancer is in part coordinated by extracellular vesicles (EVs) secreted by cancer cells. In this paper the authors found that cancer-derived EVs can stimulate endothelial cell migration and tube formation independently of uptake.These responses were mediated by the 189 amino acid isoform of vascular endothelial growth factor (VEGF) on the surface of sEVs. Unlike other common VEGF isoforms, VEGF189 preferentially localized to sEVs through its high affinity for heparin. Interaction of VEGF189 with the surface of sEVs profoundly increased ligand half-life and reduced its recognition by the therapeutic VEGF antibody bevacizumab. sEV-associated VEGF (sEV-VEGF) stimulated tumor xenograft growth but was not neutralized by bevacizumab. Furthermore, high levels of sEV-VEGF were associated with disease progression in bevacizumab-treated cancer patients, raising the possibility that resistance to bevacizumab might stem in part from elevated levels of sEV-VEGF.
To read the full article go HERE.