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EGFR — 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

Maity et al., Cancer Res 2000 (Glioblastoma) : Pharmacological inhibition of EGFR , Ras, or PI(3) kinase, but not MAP kinase, led to a significant decrease in VEGF mRNA levels in U87 MG cells ... Therefore, in glioblastoma cells, transcriptional regulation of the VEGF promoter by EGFR appears to involve Ras/PI(3) kinase and to be distinct from signals induced by hypoxia
Fujiyama et al., Circ Res 2001 : Ang II also upregulated vascular endothelial growth factor ( VEGF ) expression in an HB-EGF/EGFR dependent manner
O-charoenrat et al., Clin Exp Metastasis 2000 (Carcinoma, Squamous Cell...) : One mechanism may be potentiation of angiogenesis, since upregulation of vascular endothelial growth factor ( VEGF ) expression by activation of epidermal growth factor receptor (EGFR) and/or c-erbB-2 has been described
Clarke et al., Br J Cancer 2001 (Cell Transformation, Neoplastic) : Mutant epidermal growth factor receptor enhances induction of vascular endothelial growth factor by hypoxia and insulin-like growth factor-1 via a PI3 kinase dependent pathway ... These results show that the mutant EGFR interacts with other growth factors and hypoxia to regulate VEGF via a PI3 kinase pathway, and suggests a specific role for anti-mutant EGFR antibodies and PI3 kinase inhibitors as therapy of this specific tumour target
Viloria-Petit et al., Cancer Res 2001 (Carcinoma, Squamous Cell...) : Because of the reported suppressive effect of EGFR inhibitors on vascular endothelial growth factor ( VEGF ) expression, and the demonstrated role of VEGF in the angiogenesis and growth of A431 tumor xenografts, relative VEGF expression was examined
Tebbutt et al., Eur J Cancer 2002 (Colorectal Neoplasms) : Farnesyl transferase inhibition, inhibition of the epidermal growth factor receptor (EGFR) and the vascular endothelial growth factor ( VEGF ) are undergoing evaluation in advanced disease
Bancroft et al., Int J Cancer 2002 (Carcinoma, Squamous Cell...) : We conclude that antagonists of EGFR, PI3K and MEK signal pathways have inhibitory activity against EGFR induced NF-kappaB and AP-1 activation, IL-8 and VEGF expression and growth by HNSCC
Casanova et al., Cancer Res 2002 (Cell Transformation, Neoplastic...) : This study reports that activated Ha-ras results in a dramatic induction of EGFR in epidermal tumor cells and provides experimental evidence that EGFR signaling is responsible for Ha-ras dependent vascular endothelial growth factor ( VEGF ) induction, as well as for the repression of other angiogenic factors such as angiopoietin 1
Li et al., Clin Cancer Res 2002 (Carcinoma, Squamous Cell...) : In vitro studies demonstrated that EGFR inhibition by antisense oligonucleotides or EGFR-specific tyrosine kinase inhibitor down-regulated the production of VEGF in HNSCC cells
Pore et al., Cancer Res 2003 (Glioblastoma) : PTEN mutation and epidermal growth factor receptor activation regulate vascular endothelial growth factor ( VEGF ) mRNA expression in human glioblastoma cells by transactivating the proximal VEGF promoter ... The effect of EGFR activation on VEGF was mediated at the level of transcription via a phosphatidylinositol 3'-kinase (PI3K) dependent pathway
Spinella et al., J Biol Chem 2004 (Disease Progression...) : At the mechanistic level, we prove that the induction of PGE2 and VEGF by ET-1 involves Src mediated epidermal growth factor receptor transactivation
Sini et al., Clin Cancer Res 2005 (Neoplasms, Experimental) : The antitumor and antiangiogenic activity of vascular endothelial growth factor receptor inhibition is potentiated by ErbB1 blockade ... In vitro, ErbB1 inhibition blocked VEGF release by tumor cells and proliferation of both tumor and endothelial cells
Semino et al., Exp Cell Res 2006 : We show here that autocrine ligand activation of epidermal growth factor (EGF) receptor in combination with interstitial flow is critically involved in the morphogenetic response of endothelial cells to VEGF stimulation
Soma et al., Int J Cancer 2006 (Disease Progression...) : In vitro, CDCA induced the production of PGE2 and VEGF in dose- and time dependent manners, and these effects were attenuated by a selective COX-2 inhibitor, mitogen activated protein kinases inhibitor, or epidermal growth factor receptor inhibitor
Younes et al., Clin Cancer Res 2006 (Adenocarcinoma, Follicular...) : Dual epidermal growth factor receptor and vascular endothelial growth factor receptor inhibition with NVP-AEE788 for the treatment of aggressive follicular thyroid cancer
Li et al., Int J Mol Med 2006 : EGFR kinase inhibitor, PD153035, inhibited UV-induced HIF-1alpha and VEGF protein expression in a dose dependent manner
Tabernero et al., Mol Cancer Res 2007 (Neoplasms) : Close relationships between these factors exist : VEGF signaling is up-regulated by EGFR expression and, conversely, VEGF up-regulation independent of EGFR signaling seems to contribute to resistance to EGFR inhibition
Damiano et al., Proc Natl Acad Sci U S A 2007 (Colonic Neoplasms) : VEGF is activated by EGFR , and its overexpression causes resistance to EGFR inhibitors
Yoshikawa et al., Br J Cancer 2008 (Bile Duct Neoplasms...) : These results suggest that EGFR expression is associated with tumour progression and VEGF expression may be involved in haematogenic metastasis in cholangiocarcinoma
Basu et al., J Biol Chem 2008 (Stomach Neoplasms) : We demonstrate that the H. pylori secretory protein, HP0175, by virtue of its ability to bind TLR4, transactivates EGFR and stimulates EGFR dependent VEGF production in the gastric cancer cell line AGS ... Knock-out of the hp0175 gene attenuates the ability of the resultant H. pylori strain to activate EGFR or to induce VEGF production
Cohen-Kaplan et al., Cancer Res 2008 (Carcinoma, Squamous Cell...) : Thus, heparanase seems to modulate two critical systems involved in tumor progression, namely VEGF expression and EGFR activation
Flaig et al., BJU Int 2009 (Urinary Bladder Neoplasms) : Dual epidermal growth factor receptor and vascular endothelial growth factor receptor inhibition with vandetanib sensitizes bladder cancer cells to cisplatin in a dose- and sequence dependent manner
Tournigand et al., Rev Med Interne 2009 (Colorectal Neoplasms...) : Recent phase III trials demonstrated a significant clinical benefit with bevacizumab, a VEGF inhibitor , and with EGFR-inhibitors , namely cetuximab and panitumumab
Flores et al., Journal of carcinogenesis 2009 : Likewise, in the tumor homogenate the mean VEGF expression was higher at 60 min post-goserelin administration than the basal levels, although VEGF expression then diminished at 90 min. Plasma EGFR expression was higher in rats with NMU induced tumors than in healthy controls ( P Conclusions : The results allow us to conclude that goserelin may exert a short-term stimulatory effect on the release of VEGF , as well as a long-term inhibitory effect on VEGF but not EGFR expression
Kargiotis et al., J Neurooncol 2010 (Anoxia...) : Activation of cell surface receptors, such as the epidermal growth factor receptor , utilization of signaling pathways, and over-expression of cytokines, proteases and growth factors, for example the matrix metalloproteinases and vascular endothelial growth factor , protect tumor and non-tumor cells from apoptosis, increase their ability to invade to adjacent or distant areas, and trigger angiogenesis
Ye et al., Oncogene 2010 (Neoplasms) : In conclusion, anti-Axl mAb can enhance the therapeutic efficacy of anti-VEGF , EGFR small-molecule inhibitors as well as chemotherapy
Shih et al., Cancer Res 2010 (Neovascularization, Pathologic...) : Notably, modulation of VEGF expression by DLC1 was dependent on epidermal growth factor receptor-MAP/ERK kinase-hypoxia-inducible factor 1 signaling but on RhoA pathways
Luangdilok et al., Eur J Cancer 2011 (Carcinoma, Squamous Cell...) : The addition of exogenous EGF induced the expression of VEGF-C and VEGF-A in a concentration dependent manner and this was blocked by a selective EGFR inhibitor, gefitinib ... In both cell lines stimulated with endogenous or exogenous ligand, inhibition of MEK1/2 ( with U0126 or PD98059 ) or PI3K ( with PI-103 or LY294002 ) resulted in a marked reduction of EGFR induced VEGF-A expression, whereas exogenous EGF induced VEGF-C upregulation was blocked by inhibitors of MEK but not PI3K ... Taken together, our evidence suggests that both endogenous and exogenous EGFR activation induces VEGF-A expression requiring both PI3K and MAPK signalling whereas VEGF-C expression is dependent on MAPK, but not the PI3K or mTOR pathways in SCCHN cell lines
Wachsberger et al., Int J Radiat Oncol Biol Phys 2012 (Glioblastoma) : The presence of EGFR augmented RT-stimulated VEGF release ; this effect was inhibited by vandetanib
Martin et al., Eur Respir J 2011 (Bronchiectasis...) : Because epidermal growth factor receptor (EGFR) activation regulates VEGF synthesis in cancer, we also evaluated the roles of EGFR ... Persistent PA infection induced VEGF synthesis in airway epithelium and peribronchial angiogenesis, at least in part via EGFR dependent mechanisms
Zhang et al., Int J Cancer 2012 (Head and Neck Neoplasms...) : DT-IgG suppressed Tu212 and A549 cell growth, inhibited EGFR activation and induced apoptosis as effectively as cetuximab, and neutralized VEGF as effectively as bevacizumab ... DT-IgG induced EGFR dependent VEGF internalization, constituting a novel antiangiogenesis mechanism
Juárez-Verdayes et al., Graefes Arch Clin Exp Ophthalmol 2013 : Peptidoglycan and muramyl dipeptide from Staphylococcus aureus induce the expression of VEGF-A in human limbal fibroblasts with the participation of TLR2-NF?B and NOD2-EGFR
Tsao et al., J Thorac Oncol 2013 (Carcinoma, Non-Small-Cell Lung...) : Although vandetanib is no longer in development in NSCLC, identification of a molecular phenotype that responds to dual epidermal growth factor receptor and vascular endothelial growth factor receptor inhibition would contribute to the field
Fernández-Martínez et al., Biochim Biophys Acta 2013 : Thus, EGFR transactivation by intracellular PGE2 activated EP receptors results in the sequential activation of RARß and HIF-1a leading to increased production of VEGF-A and it may be a target for the therapeutic modulation of HIF-1a/VEGF-A
Goldman et al., Mol Biol Cell 1993 (Brain Neoplasms...) : Specifically, EGF activation of EGFr expressed on glioma cells leads to enhanced secretion of VEGF by glioma cells