Figures & data
Figure 1 Schematic representation of how the VEGF-A signaling pathway is linked to its main biological functions.
Notes: VEGF-A can bind VEGFR-2 dimer. NRP-1 and -2 are co-receptors that stabilize the VEGFR-2 dimer. Upon ligand binding to VEGFR-2 dimer, several signaling pathways can be activated, affecting diverse biological processes in endothelial and cancer cells. Anti-VEGF-A mAbs, such as bevacizumab or the fusion protein aflibercept, can bind to VEGF-A and block its function.
Abbreviations: mAb, monoclonal antibody; NRP, neuropilin; VEGF, vascular endothelial growth factor; VEGFR, VEGF receptor; PKC, protein kinase C; PLC, phospholipase C; FAK, focal adhesion protein; TSAd-Src, T cell-specific adaptor protein containing an Src homology.
Abbreviations: mAb, monoclonal antibody; NRP, neuropilin; VEGF, vascular endothelial growth factor; VEGFR, VEGF receptor; PKC, protein kinase C; PLC, phospholipase C; FAK, focal adhesion protein; TSAd-Src, T cell-specific adaptor protein containing an Src homology.
Figure 2 An overview of the EGFR pathway and its main downstream effectors, PI3K/AKT and KRAS/BRAF/MEK/MERK.
Notes: Activated AKT and MEK/MERK can induce cancer cell proliferation and invasion. In addition, activated AKT can induce cancer stem cell renewal and differentiation. Anti-EGFR mAbs, such as cetuximab or panitumumab, can bind EGFR and block its function.
Abbreviations: EGFR, epidermal growth factor receptor; mAb, monoclonal antibody; CSC, cancer stem cell.
Abbreviations: EGFR, epidermal growth factor receptor; mAb, monoclonal antibody; CSC, cancer stem cell.
