Table 1.
Effects of VEGF/VEGFR autocrine-paracrine signaling in cancer cells.
| Cancer Type | Effects |
|---|---|
| Melanoma (VEGFR1/2; NRP1/2) |
Enhances the proliferation of melanoma cells [59]. Mitigates melanoma cells migration (through a NRP1/VEGFR2-mediated response) [60]. |
| Pancreatic (VEGFR1/2; NRP1) |
Was shown to activate the MAPK/ERK pathway [44,61]. Stimulates cancer cell growth [44]. Promotes cancer cell migration and invasion, without affecting proliferation (VEGFR1-mediated effect) [61]. Promotes pancreatic cancer aggressiveness by TGFβ1-induced fibrosis and endothelial-to-mesenchymal transition (NRP1-mediated effect) [62]. |
| NSCLC (VEGFR1/2; NRP1/2) |
Induces PI3K/Akt and MAPK/ERK activation [63]. Stimulates tumor growth and proliferation of NRP1-expressing cells (VEGFR2/NRP1-mediated effect) [63]. |
| SCLC (VEGFR2/3) |
Promotes VEGFR2/3 activation resulting MAPK/ERK phosphorylation [64]. Induces cancer cell proliferation [64]. |
| Colorectal (VEGFR1) |
Promotes Akt and ERK phosphorylation [65]. Enhances survival and resistance to chemotherapy of cancer cells [65]. Was shown to enhance cellular migration and promote tumor progression and metastasis [66,67]. Was found to support the survival of cancer cells undergoing EMT [68,69]. |
| Gastric (VEGFR1/2) |
Stimulates tumor growth (VEGFR2-mediated response) [57,70]. |
| Prostate (VEGFR1/2) |
Was shown to enhance prostate cancer cells proliferation (VEGFR2-mediated effect) [71,72]. |
| Glioblastoma (VEGFR1/2; NRP1) |
Promotes MAPK/ERK, PI3K/Akt and PLC/PKC pathways activation [73,74]. Stimulates proliferation of glioma cells (VEGFR2-mediated response) [75]. Supports tumor growth (VEGFR1/2-mediated effect) [73]. |
| Breast cancer (VEGFR1/2; NRP1) |
Induces activation of the MAPK/ERK and PI3K/Akt pathways [76]. Supports tumor cells survival, stimulates their proliferation and contributes to mammary tumor growth [77,78,79,80,81]. Induces invasion and chemotaxis of breast cancer cells and enhances EMT [79,80,81,82]. Inhibits apoptosis and protects from chemotherapy [79,83]. Confers cancer stem cells traits in breast cancer cells and was found to drive cancer stem cells self-renewal [84,85]. |
| Head & Neck (VEGFR2) |
Regulates proliferation and invasion of head & neck cancer cells [86]. |
| Bladder (VEGFR1/2) |
Enhances survival and proliferation of bladder cancer cells (VEGFR2-mediated effect) [45,87]. |
| Rhabdomyosarcoma (VEGFR1/2) |
Increases cancer cell proliferation (VEGFR1-mediated effect) [52]. |
| Ovarian (VEGFR2) |
VEGFR2-phosphorylation has been corelated with ovarian cancer cell survival and proliferation [58]. |
| Multiple Myeloma (VEGFR1) |
Mediates activation of the MAPK/ERK, PI3 k/PKC and McL1/survivin pathways resulting in increased proliferation, migration and survival [88,89,90,91,92]. |
Abbreviations: EMT: epithelial–mesenchymal transition; VEGF(R): vascular endothelial growth factor (receptor); NRP: neuropilin; MAPK: Mitogen-activated protein kinase; ERK: extracellular signal-regulated kinase; TGFβ1: Transforming growth factor beta 1; PI3K: Phosphoinositide 3-kinase; Akt: Protein kinase B; PLC:phospholipase C; PKC: Protein kinase C; McL1: myeloid cell leukemia 1.