Gene interactions and pathways from curated databases and text-mining

◀ Back to VEGFA

SRC — VEGFA

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Wiener et al., Clin Cancer Res 1999 (Disease Models, Animal...) : Furthermore, this evidence suggests that as in other tumor systems, Src activity is required for vascular endothelial growth factor induction and angiogenic development
Pal et al., Cancer Res 2001 (Breast Neoplasms) : The present study indicates that p53 can also inhibit the hypoxic induction of Src kinase activity and thereby may prevent VPF/VEGF transcription
Eliceiri et al., J Cell Biol 2002 : We find that VEGF stimulated Src activity in chick embryo blood vessels induces the coupling of focal adhesion kinase ( FAK ) to integrin alpha(v)beta5, a critical event in VEGF mediated signaling and biological responsiveness
Niu et al., Oncogene 2002 (Neovascularization, Pathologic) : Consistent with an important role of Stat3 in VEGF up-regulation induced by various oncogenic tyrosine kinases, v-Src mediated VEGF expression is inhibited when Stat3 signaling is blocked ... Moreover, chromatin immunoprecipitation assays indicate that Stat3 protein binds to the VEGF promoter in vivo and mutation of a Stat3 binding site in the VEGF promoter abrogates v-Src induced VEGF promoter activity
Yin et al., FASEB J 2003 (Cell Transformation, Neoplastic...) : Specific inhibitors of protein kinase C ( PKC ), Src , and phosphatidylinositol 3-kinase (PI3K) inhibit Par1 induced VEGF expression, suggesting the participation of these kinases in the process
Anand et al., Biol Reprod 2003 (MAP Kinase Signaling System) : A specific Src kinase inhibitor, PP2, could completely block the stimulatory effects of both gonadotropin and 8Br-cAMP on VEGF production by Leydig cells, implying an involvement of the Src kinase pathway
Gruden et al., Kidney Int 2003 : IGF-I induces vascular endothelial growth factor in human mesangial cells via a Src dependent mechanism ... IGF-I induces VEGF gene expression and protein secretion in human mesangial cells via a Src dependent mechanism
Fukuda et al., Cancer Res 2003 (Colonic Neoplasms) : Inhibition of C-SRC tyrosine kinase activity also blocks PGE ( 2 ) -induced HIF-1alpha protein and VEGF mRNA expression without blocking ERK phosphorylation
Laird et al., Mol Cancer Ther 2003 (Neoplasms, Experimental) : Src family kinase activity is required for signal tranducer and activator of transcription 3 and focal adhesion kinase phosphorylation and vascular endothelial growth factor signaling in vivo and for anchorage dependent and -independent growth of human tumor cells
Lin et al., Mol Pharmacol 2003 : In addition, antioxidant N-acetyl-cysteine was demonstrated to strongly inhibit VEGF mediated Src activation , VE-cadherin tyrosine phosphorylation, and HUVEC tube formation
Weis et al., J Cell Biol 2004 (Neoplasm Metastasis...) : Endothelial barrier disruption by VEGF mediated Src activity potentiates tumor cell extravasation and metastasis
Gray et al., Oncogene 2005 (Anoxia...) : HIF-1alpha, STAT3, CBP/p300 and Ref-1/APE are components of a transcriptional complex that regulates Src dependent hypoxia induced expression of VEGF in pancreatic and prostate carcinomas ... In normal fibroblasts, hypoxia induced activation of the protein tyrosine kinase, Src , is required for VEGF expression ... Expression of activated Src from an inducible promoter is sufficient to increase VEGF expression and form these STAT3/HIF-1alpha containing promoter complexes ... We show here in both pancreatic and prostate carcinoma cell lines cobalt chloride ( used to mimic hypoxia ) -induced VEGF expression requires Src activation and leads to increased steady-state levels of HIF-1alpha and increased phosphorylation of signal and transducer of transcription 3 ( STAT3 )
Yonezawa et al., Mol Carcinog 2005 (Kidney Neoplasms...) : Furthermore, in Caki-1 cells with higher Src activity, Src stimulated the production of vascular endothelial growth factor ( VEGF ), partially via the activation of Stat3, and the inhibition of Src activity caused a reduction of the VEGF level in serum, angiogenesis, and tumor development in a xenograft model
Mariappan et al., J Biol Chem 2005 : VEGF induced Erk activation was not dependent on phosphoinositide (PI) 3-kinase activation but required sequential phosphorylation of type 2 VEGF receptor, PLCgamma and c-Src , as demonstrated by inhibitors SU1498, U73122, and PP1, respectively ... VEGF also stimulated phosphorylation of Pyk-2 ; VEGF induced phosphorylation of Pyk2, c-Src and Raf-1 could be abolished by BAPTA/AM, demonstrating requirement for induction of intracellular calcium currents
Ali et al., J Pharmacol Sci 2005 : M475271 inhibited VEGF induced Flk-1 and Src phosphorylation and their association
Summy et al., Pancreas 2005 (MAP Kinase Signaling System...) : c-Src regulates constitutive and EGF mediated VEGF expression in pancreatic tumor cells through activation of phosphatidyl inositol-3 kinase and p38 MAPK ... The goal of this study was to determine the role of Src in regulating VEGF expression and angiogenic potential in pancreatic cancer cell lines ... Src activity contributes to constitutive and EGF induced VEGF expression and angiogenic potential in pancreatic cancer cells
Chao et al., Oncogene 2007 (Gastrointestinal Neoplasms...) : Enhanced tumorigenicity of CCK ( 2i4sv ) R is associated with an Src dependent increase in the transcription factor, hypoxia-inducible factor-1alpha, its downstream target, vascular endothelial growth factor and tumor micro-vessel density, suggesting that CCK ( 2i4sv ) R may contribute to the growth and spread of GI cancers through agonist independent mechanisms that enhance tumor angiogenesis
Kanda et al., Cell Signal 2007 : Ang1 upregulated the Src dependent secretion of vascular endothelial growth factor-A ( VEGF-A ) ... Taken together, our results suggest that Ang1 induces capillary morphogenesis in HUVECs through Src dependent upregulation of endogenous VEGF-A
Han et al., Cancer Res 2006 (Ovarian Neoplasms) : In addition, Src inhibition alone and in combination with docetaxel significantly down-regulated tumoral production of vascular endothelial growth factor and interleukin 8, whereas combination therapy decreased the microvessel density ( P = 0.02 ) and significantly affected vascular permeability ( P < 0.05 )
Donnini et al., Int J Cancer 2007 (Carcinoma, Squamous Cell...) : In cultured endothelial cells, 1l inhibited the VEGF induced phosphorylation on tyr416 of c-Src , resulting in a reduced cell proliferation and invasion
El-Remessy et al., FASEB J 2007 : The specific peroxynitrite decomposition catalyst FeTPPs blocked VEGF induced phosphorylation of VEGFR2 and c-Src and inhibited endothelial cell migration and tube formation
Herynk et al., J Exp Ther Oncol 2007 (Colorectal Neoplasms...) : Additionally, the Src selective inhibitor, PP2, significantly reduced basal VEGF production in KM20 parental cells, and this effect could be rescued by HGF treatment
Mahabeleshwar et al., Circ Res 2007 : VEGF stimulated recruitment and activation of c-Src and subsequent beta3 integrin tyrosine phosphorylation are critical for interaction between VEGFR-2 and beta3 integrin
Matsui et al., Circulation 2007 (Ischemia) : PI3-kinase is associated with vascular endothelial growth factor induced PYK2/Src complex, and inhibition of Src blocked Akt activation
Kinney et al., Am J Physiol Cell Physiol 2008 : A Src kinase inhibitor ( PP1 ) completely blocked both VEGF- and thrombin induced MKP-1 expression
Acevedo et al., Blood 2008 : While both Sema3A- and VEGF induced VP was Nrp-1 dependent, they use distinct downstream effectors since VEGF- but not Sema3A induced VP required Src kinase signaling
Cheranov et al., Blood 2008 : 14,15-EET induced the expression of vascular endothelial cell growth factor ( VEGF ) in a time- and Src-STAT-3 dependent manner in HDMVECs ... These results reveal that Src dependent STAT-3 mediated VEGF expression is a major mechanism of 14,15-EET induced angiogenesis
Singleton et al., Mol Cancer Ther 2008 : Silencing receptor protein tyrosine phosphatase mu expression ( small interfering RNA ) in human EC inhibited both synergy between MNTX and bevacizumab or 5-FU and increased VEGF induced tyrosine phosphorylation of Src and p190 RhoGAP with enhanced activation of Akt and the actin cytoskeletal regulatory protein, RhoA, whereas silencing Src, Akt, or RhoA blocked VEGF induced angiogenic events
Bhattacharya et al., Journal of molecular signaling 2008 : Furthermore, we identified Src as an important target for dopamine mediated inhibition of VPF/VEGF induced permeability
Fan et al., Mol Cancer Ther 2008 (Colorectal Neoplasms) : Inhibition of Akt or Src activation with wortmannin or PP2 blocked induction of VEGF-A by oxaliplatin in HT29 or RKO cells, respectively
Liang et al., J Pharmacol Exp Ther 2009 (Brain Ischemia...) : Our results demonstrate that both agents potently block VEGF mediated signaling in human endothelial cells, penetrate rat brain upon systemic administration, and inhibit postischemic Src activation and vascular leakage
Sheikpranbabu et al., Journal of nanobiotechnology 2009 : We report that VEGF and IL-1beta-stimulate endothelial permeability via Src dependent pathway by increasing the Src phosphorylation and Ag-NP block the VEGF-and IL-1beta induced Src phosphorylation at Y419
Zhang et al., Blood 2010 (Retinal Neovascularization) : Furthermore, siRNA mediated down-regulation of VEGF inhibited hypoxia induced Src-PLD1-PKCgamma activation and neovascularization
Liao et al., Endocrinology 2010 : Caveolin-1 down-regulation suppressed VEGF stimulated phosphorylation of Akt, JNK, eNOS, c-Src , and FAK ; however, basal activities of c-Src and FAK were elevated in parallel with increased stress fiber formation and focal adhesion ... Caveolin-1 overexpression also inhibited VEGF induced phosphorylation of Akt, JNK, c-Src , FAK, and eNOS
Lee et al., FEBS Lett 2010 : We demonstrate that reduction in Ca ( 2+ ) by chelating compound BAPTA-AM or by IP ( 3 ) -endoplasmic reticulum blocker 2-APB selectively inhibited VEGF induced activation of c-Src-PI3K-Akt but not ERK1/2 in human coronary artery endothelial cells ( HCAEC ) ... We also show that the selective inhibitory effects of NADPH oxidase knockdown on VEGF mediated activation of c-Src-PI3K-Akt signaling and cell proliferation in HCAEC can be reversed by increase in intracellular Ca ( 2+ )
Moreno-Smith et al., Clin Cancer Res 2011 (Neovascularization, Pathologic...) : Moreover, dopamine reduced cyclic AMP levels and inhibited norepinephrine and vascular permeability factor/VEGF induced Src kinase activation
Lee et al., PloS one 2011 : Co-immunoprecipitation studies using human coronary artery ECs ( HCAEC ) showed that VEGF induced ROS dependent interaction between VEGFR-2 and c-Src correlated with their thiol oxidation status
Ruan et al., EMBO J 2012 : Upon VEGF-A dependent activation of VEGF receptor-2 (VEGFR-2), and subsequent TSAd mediated activation of Src family kinases (SFKs) , SFKs engage the receptor tyrosine kinase Axl via its juxtamembrane domain to trigger ligand independent autophosphorylation at a pair of YXXM motifs that promotes association with PI3K and activation of Akt
Sun et al., J Exp Med 2012 (Extravasation of Diagnostic and Therapeutic Materials) : c-Src was activated in vivo and in vitro in a VEGF/TSAd dependent manner, and was regulated via increased phosphorylation at pY418 and reduced phosphorylation at pY527 ... Tsad silencing blocked VEGF induced c-Src activation, but did not affect pathways involving phospholipase C?, extracellular regulated kinase, and endothelial nitric oxide
Singh et al., Blood 2013 (Anoxia...) : To understand the mechanisms of Src-PLD1-PKC?-cPLA activation by vascular endothelial growth factor A ( VEGFA ), we studied the role of Kdr and Flt1 ... Depletion of Kdr attenuated VEGFA induced Src-PLD1-PKC?-cPLA activation ... Regardless of its phosphorylation state, downregulation of Flt1 also inhibited VEGFA induced Src-PLD1-PKC?-cPLA activation, but only modestly ... Furthermore, depletion of VEGFA or VEGFB attenuated hypoxia induced Src-PLD1-PKC?-cPLA activation and retinal neovascularization ... These findings suggest that although VEGFA, through Kdr and Flt1, appears to be the major modulator of Src-PLD1-PKC?-cPLA signaling in HRMVECs, facilitating their angiogenic events in vitro, both VEGFA and VEGFB mediate hypoxia induced Src-PLD1-PKC?-cPLA activation and retinal neovascularization via activation of Kdr and Flt1, respectively
Rajpar et al., Cancer J 2013 (Bone Neoplasms...) : Different drugs are available or in development that target bone resorption ( bisphosphonates, RANK ligand inhibitors ), bone formation ( endothelin 1 inhibitors ), cancer cell migration ( SRC-family kinase inhibitors, vascular endothelial growth factor-MET inhibitors ), and survival ( radiopharmaceuticals )
Wang et al., Mol Cell Biol 2013 (Disease Models, Animal...) : Upregulation of CD146 facilitated an endothelial response to VEGF induced SRC kinase family (SKF)/p38 mitogen activated protein kinase ( MAPK ) /NF-?B activation and consequently promoted endothelial cell migration and tube formation
Mukhopadhyay et al., Nature 1995 (Neovascularization, Pathologic) : Expression of either a dominant negative mutant form of c-Src or of Raf-1 markedly reduces VEGF induction
Mukhopadhyay et al., Cancer Res 1995 (Neovascularization, Pathologic) : Here we have studied the role of p53, a tumor suppressor, and v-Src , an oncogene on VEGF regulation
Fleming et al., Surgery 1997 (Adenocarcinoma...) : Recently we demonstrated that decreased activity of pp60c-src in colon tumor cells contributes to decreased expression of VEGF