◀ Back to VEGFA

MET — VEGFA

Pathways - manually collected, often from reviews:

• KEGG Focal adhesion: EGF/FIGF/HGF/IGF1/PDGFA/PDGFB/PDGFC/PDGFD/PGF/VEGFA/VEGFB/VEGFC → EGFR/ERBB2/FLT1/FLT4/IGF1R/KDR/MET/PDGFRA/PDGFRB (protein-protein, activation)
  
• WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway: EFNA1/FGF1/FGF11/FGF10/EFNA2/EGF/FGF12/CSF1/ANGPT4/ANGPT2/ANGPT1/VEGFA/EFNA3/EFNA4/EFNA5/FGF14/FGF19/FGF17/FGF18/FGF2/FGF3/FGF4/FGF6/FGF7/FGF8/FGF9/FIGF/HGF/IGF1/INS/INS/KITLG/VEGFC/VEGFB/PDGFB/PGF/PDGFA/NGF/PDGFC/FGF21/FGF22/PDGFD/FGF20/FGF16 → FGFR2/KDR/INSR/FGFR3/IGF1R/KIT/FGFR1/EPHA2/EGFR/CSF1R/FGFR4/FLT1/FLT4/NGFR/MET/PDGFRA/PDGFRB/TEK (activation)
  
• WikiPathways Focal Adhesion: EGF/FIGF/HGF/IGF1/PDGFA/PDGFB/PGF/PDGFC/PDGFD/VEGFA/VEGFB/VEGFC → BLK/EGFR/ERBB2/FGR/FLT1/HCK/IGF1R/KDR/MET/PDGFRA/PDGFRB/PTK6/SRMS/TXK/TESK2/STYK1/TNK2/TNK1 (activation)
  

Text-mined interactions from Literome

Kuba et al., Cancer Res 2000 (Carcinoma, Lewis Lung...) : HGF and VEGF activated the Met/HGF receptor and the KDR/VEGF receptor, respectively, whereas NK4 inhibited HGF induced Met tyrosine phosphorylation but not VEGF induced KDR phosphorylation
Saucier et al., Proc Natl Acad Sci U S A 2004 (Neoplasms...) : The Shc adaptor protein is critical for VEGF induction by Met/HGF and ErbB2 receptors and for early onset of tumor angiogenesis
Zhang et al., Molecular cancer 2010 (Bone Neoplasms...) : Intriguingly, VEGF165 promoted physical interaction between NRP1 and hepatocyte growth factor (HGF) receptor c-MET , and facilitated c-MET phosphorylation via a NRP1 dependent mechanism
Torres et al., Clin Cancer Res 2011 (Neoplasm Invasiveness...) : MET activation increased MPNST cell motility, invasion, angiogenesis, and induced matrix metalloproteinase-2 (MMP2) and VEGF expression ; MET knockdown had inverse effects in vitro and markedly decreased local and metastatic growth in vivo
Neill et al., J Biol Chem 2012 (Neovascularization, Pathologic) : Decorin antagonizes the angiogenic network : concurrent inhibition of Met , hypoxia inducible factor 1a, vascular endothelial growth factor A, and induction of thrombospondin-1 and TIMP3
Lu et al., Cancer Cell 2012 (Brain Neoplasms...) : Consequently, VEGF blockade restores and increases MET activity in GBM cells in a hypoxia independent manner, while inducing a program reminiscent of epithelial-to-mesenchymal transition highlighted by a T-cadherin to N-cadherin switch and enhanced mesenchymal features
Xie et al., Future Oncol 2012 : In this article, Lu et al. reported a novel mechanism whereby VEGF negatively regulates tumor cell invasion by blocking MET phosphorylation in the MET/VEGFR2 complex ... They showed that inhibiting the VEGF pathway results in MET activation in VEGF-knockout mouse models and in patients after bevacuzimub treatment, and that MET knockdown blocked the invasiveness of VEGF knockout tumors, suggesting that blocking the MET pathway can prevent post-bevacizumab treatment tumor recurrence, providing a strong rationale for using a combination of MET and VEGF receptor inhibitors to treat glioblastoma patients
Soda et al., J Mol Med (Berl) 2013 (Glioblastoma...) : Enhanced invasiveness is one such resistance mechanism and recent works report the contribution of activated MET signaling induced by inhibition of VEGF signaling
Sennino et al., Cancer Res 2013 (Lymphatic Metastasis...) : In particular, we examined whether c-Met is upregulated in lymphatics in or near pancreatic neuroendocrine tumors in RIP-Tag2 transgenic mice and whether lymph node metastasis can be reduced by concurrent inhibition of VEGF and c-Met signaling ... Together, these results indicate that inhibition of VEGF signaling in RIP-Tag2 mice upregulates c-Met expression in lymphatic endothelial cells, increases the number of intratumoral lymphatics and number of tumor cells within lymphatics, and promotes metastasis to local lymph nodes