“…In this way, NRP1 and 2 interact with SEMA3 membrane-associated receptors located in the central nervous system (plexins) and their growth factors (class 3 semaphorins) [101][102][103]. In addition, they bind to a series of growth factor s and their receptors, including VEGF/VEGFR [75,76,[104][105][106], TGF-β1/TGFβ1R [107,108], HGF/c-Met [109,110], PDGF/PDGFR [111][112][113], FGFs/FGFR [112,[114][115][116][117], EGF/EGFR, BDNF/ TRKA,B [118] as well as IGF/INSR [119]. These interactions favor the growth of potential tumor cells (Figure 3a (growth factor) receptors including (from left to right) PTK7 (pseudo tyrosine kinase, receptor7, CCK4), VEGFR1/2/3 (vascular endothelial growth factor receptor 1/2/3), PDGFRα/β ( platelet derived growth factor receptor α/β; CSF1R, KIT, FLK2), FGFR1/2/3/4 (fibroblast growth factor receptor 1/2/3/4), c-Met (tyrosine-protein kinase Met or hepatocyte growth factor receptor (HGFR); Ron, Sea), TrKA/B (tropomyosin receptor kinase A/B), RORα/β (RAR (retinoic acid receptor)-related orphan receptor-α/β), MuSK (muscle-specific kinase), TieR1/2 (tyrosine kinase with immunoglobulin-like and EGF-like domains 1/2, angiopoietin receptor), and AXL (AXL receptor tyrosine kinase).…”