Gene interactions and pathways from curated databases and text-mining

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EGF — PIK3CA

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Okano et al., J Biol Chem 2000 (Esophageal Neoplasms) : Robust activation of Akt2 by EGF was observed in some cell lines in a PI3K dependent manner
Dufourny et al., J Endocrinol 2000 (Breast Neoplasms) : Since transcriptional activation of the cyclin D1 promoter by EGF , E2 and TPA is independent of PI3-K activity, these findings suggest a post-transcriptional role for PI3-K in the regulation of cyclin D1 expression
Wu et al., Oncogene 2000 (Brain Neoplasms...) : Reduced EGF stimulated activation of PI3-K was mediated by interactions between carboxyl terminus of SIRPalpha1 and the Src homology-2 (SH2) containing phosphotyrosine phosphatase, SHP2
Chen et al., EMBO Rep 2001 : However, in this report we demonstrate that inhibition of epidermal growth factor (EGF) stimulated PI3K activity by expression of the kinase-deficient PI3K p110 subunit ( p110delta kin ) does not block the lysosomal targeting and degradation of the EGF receptor (EGFR)
Zhong et al., Biochem Biophys Res Commun 2001 (Prostatic Neoplasms) : Compared to that of HIF-1alpha, the constitutive, serum-, EGF- , and PMA increased HIF-1beta protein expression were also inhibited by selective PI3K or FRAP/TOR inhibitors but in higher doses
Sbrissa et al., Mol Cell Endocrinol 2001 : Insulin but not PDGF or EGF stimulation of 3T3-L1 adipocytes markedly increased the PtdIns 3-P production ( 4.2-fold ) in PIKfyve immune complexes, primarily as a result of increased PI 3-K intrinsic enzymatic activity
Chinni et al., Clin Cancer Res 2002 : This was also accompanied by the inhibition of EGF induced phosphorylation of PI3K by I3C treatment
Zhang et al., Mol Cell Biol 2002 : Our results suggest that, in addition to its role as a positive component of the Ras-Erk pathway, Shp2 negatively regulates EGF dependent PI3K activation by dephosphorylating Gab1 p85 binding sites, thereby terminating a previously proposed Gab1-PI3K positive feedback loop
He et al., J Virol 2002 : The downstream effects of the NS5A-p85 PI3K interaction included increased tyrosine phosphorylation of p85 PI3K in response to EGF
Bonaccorsi et al., Int J Androl 2003 (Neoplasm Invasiveness...) : PI3K activity, a key signalling pathway for invasion of these cells, was decreased in PC3-AR cells in response to EGF and further reduced by treatment with R1881
Kong et al., Mol Endocrinol 2003 : In these cells, three major p85 containing complexes were formed after EGF treatment : ErbB3-p85, Shc-p85, and a multimeric Gab2-Grb2-SHP2-p85, which accounted for more than 80 % of total EGF induced PI3K activity ( Kong, M., C. Mounier, J. Wu, and B. I. Posner, J Biol Chem, 2000, 275 : 36035-36042 ) ... Overexpression of the PH domain of Gab2 did not affect EGF induced Gab2 phosphorylation, PI3K activation , and DNA synthesis ... Our data demonstrate that Gab2 mediates EGF induced PI3K activation and DNA synthesis in a PH domain independent manner
Andresen et al., Hypertension 2003 (MAP Kinase Signaling System) : We hypothesized that phosphoinositide-3-kinase (PI3K) can also act to recruit Raf to membranes ; therefore, inhibition of PI3K should inhibit EGF signaling to ERK
Koyama et al., Dev Dyn 2003 : Both PLCgamma1 and PI3K are phosphorylated in response to EGF
Li et al., Gastroenterology 2004 : EGF increased PI 3-K and active Akt2 in ileal BBM at the same time that it increased PI 3-K dependent trafficking of NHE3 to BBM and stimulation of Na absorption
Pfeil et al., Prostate 2004 (Prostatic Neoplasms) : IGF-1, EGF , and heregulin but not PDGF or activators of protein kinase A induced phosphorylation of Akt in DU145 cells and activation was completely blocked by the PI3K inhibitor LY294002
Elad-Sfadia et al., J Biol Chem 2004 : Co-transfectants of K-Ras/galectin-3, but not of H-Ras/galectin-3, exhibited enhanced and prolonged epidermal growth factor stimulated increases in Ras-GTP, Raf-1 activity, and PI3-K activity
Schiffer et al., J Biol Chem 2004 : CD2AP was not required for PI3K/AKT activation by insulin and epidermal growth factor , indicating that CD2AP is a selective mediator of anti-apoptotic TGF-beta signaling
Qiu et al., Mol Hum Reprod 2004 : mTOR/p70S6K is important in PI3K- but not MAPK mediated trophoblast migration in response to EGF
Bonaccorsi et al., J Cancer Res Clin Oncol 2004 (Prostatic Neoplasms) : In addition, we determined the effect of the compound on EGF stimulated PI3 K/AKT pathway activation, in view of the key role exerted by this pathway in carcinoma cell invasion
Bonaccorsi et al., Steroids 2004 (Neoplasm Invasiveness...) : In addition, EGF stimulated PI3K activity, a key signalling pathway for invasion of these cells, was decreased in PC3-AR cells and further reduced by treatment with R1881, indicating decreased functionality of EGFR
Bonaccorsi et al., Int J Cancer 2004 (Neoplasm Invasiveness...) : EGF stimulated PI3K activity, a key signaling pathway for invasion of these cells, and EGF-PI3K interaction are also decreased in PC3-AR cells and further reduced by treatment with androgen
Qiu et al., Reproduction 2004 (MAP Kinase Signaling System) : We showed for the first time that EGF activated both PI3K/Akt and MAPK/extracellular-signal regulated kinase ( ERK ) signalling in HTR8/SVneo, and increased both MMP-9 and TIMP-1 mRNAs and protein concentrations
Li et al., Frontiers in bioscience : a journal and virtual library 2005 (Prostatic Neoplasms) : DIM also inhibited EGFR expression, PI3K kinase activity, and Akt activation, and abrogated the EGF induced activation of PI3K in prostate cancer cells
Bonaccorsi et al., Ann N Y Acad Sci 2004 (Neoplasm Invasiveness...) : In addition, EGF stimulated PI3K activity, a key signaling pathway for invasion of these cells, was decreased in PC3-AR cells and further reduced by treatment with R1881, indicating decreased functionality of EGFR
Soodvilai et al., American journal of physiology. Renal physiology 2005 : We showed that EGF stimulation of OAT3 was reduced by inhibition of tyrosine kinase or PI3K , suggesting that they play a role in the stimulatory process ... Inhibitory effects also indicated that tyrosine kinase and PI3K are involved in the MAPK pathway for EGF stimulation of OAT3 in intact renal proximal tubules, with PI3K acting upstream and tyrosine kinase acting downstream of mitogen-activated/extracellular signal regulated kinase kinase activation
Bonaccorsi et al., Steroids 2006 (Neoplasm Invasiveness...) : In PC3-AR cells, we demonstrated a disruption of EGFR signalling properties ( reduced EGF induced EGFR autotransphosphorylation, reduced EGF stimulated PI3K activity as well as EGFR-PI3K interaction ) contributing to the lower invasive phenotype of these cells
Kim et al., Carcinogenesis 2006 (Prostatic Neoplasms) : Importantly, the degree of Akt and PI3K phosphorylations induced by EGF were also significantly suppressed
Bonaccorsi et al., Mol Cell Endocrinol 2006 (Neoplasm Invasiveness...) : EGF stimulated PI3K activity, a key signalling pathway for invasion of these cells, was decreased in PC3-AR cells and further reduced by treatment with R1881
Liu et al., Eur J Cell Biol 2006 : These results indicate that PI3K plays different roles in the activation of Ras/ERK1/2 signaling by insulin and EGF , and that insulin stimulated, but not EGF stimulated, ERK1/2 and Akt signalings diverge at PI3K
De Gregorio et al., Oncogene 2007 : This latter mutant did not affect the epidermal growth factor stimulated PI3K activity
Spillman et al., Gynecol Oncol 2007 (MAP Kinase Signaling System...) : The PI3K/Akt pathway inhibitor wortmannin decreased the amount of ser-80 MKK4 by 50 %, and inhibited EGF stimulation of MKK4 ser-80 phosphorylation by 60 %
Nakamura et al., Rheumatol Int 2007 (Sjogren's Syndrome) : EGF activates PI3K-Akt and NF-kappaB via distinct pathways in salivary epithelial cells in Sjögren 's syndrome
Mehta et al., Growth Factors 2007 (MAP Kinase Signaling System) : HB-EGF- and EGF induced HUVEC migration and capillary tube formation were dependent upon activation of PI3K , MAPK and eNOS
Cao et al., Cancer Lett 2008 (Ovarian Neoplasms) : EGF plus EGFR inhibitor primed ovarian cancer cells display increased sensitivity to taxol induced cell death, resistant to EGF induced cell migration and cell proliferation as well as ERK and PI3K/AKT activation
Holmström et al., Exp Cell Res 2008 (MAP Kinase Signaling System) : Both EGF and PDGF induced PI3K dependent Akt activation that was not involved in Erk1/2 activation
Rosenberger et al., Hum Mutat 2009 (Abnormalities, Multiple...) : Oncogenic HRAS mutations cause prolonged PI3K signaling in response to epidermal growth factor in fibroblasts of patients with Costello syndrome
Brunelli et al., J Steroid Biochem Mol Biol 2009 (Breast Neoplasms) : These findings suggest that inhibition of PI(3)K is a novel mechanism which contributes to 8PN activity to inhibit cancer cell survival and EGF induced proliferation
Watson et al., Arch Dermatol Res 2009 : PI3K-specific inhibitor LY294002 reduced EGF- and HGF stimulated chemokinesis and chemotaxis on collagen I and fibronectin
Liu et al., Int J Oncol 2010 (Prostatic Neoplasms) : Consistently, EGF and DHT stimulate Vav3 and AR interaction and enhance PI3K-Akt signaling
Edouard et al., Mol Cell Biol 2010 (LEOPARD Syndrome) : In conclusion, SHP2 mutations causing LS facilitate EGF induced PI3K/AKT/GSK-3beta stimulation through impaired GAB1 dephosphorylation, resulting in deregulation of a novel signaling pathway that could be involved in LS pathology
Sabri et al., Cell Biochem Funct 2011 (MAP Kinase Signaling System) : In this study, we investigated the effects of PI3K/AKT , ERK1/2, P38 and JNK on EGF signalling in hMSCs ... The effects of EGF on MAPKs and PI3K/AKT crosstalk were investigated by immunoblotting ; cyclooxygenase-2 (COX-2) expression was studied by real-time RT-PCR ; and cell proliferation was evaluated by methylthiazolyl tetrazolium bromide assay
Díaz et al., Cell Signal 2012 : Considering the relevance of the PI3K-Akt signaling in cell survival and in the pathogenesis of cancer, and that GH was reported to modulate EGFR expression and signaling, the objective of this study was to analyze the effects of increased GH levels on EGF induced PI3K-Akt signaling
Akl et al., Planta Med 2012 (Breast Neoplasms...) : Western blot studies revealed that combined low-dose treatment of ?-tocotrienol and sesamin caused a marked reduction in EGF induced ErbB3 and ErbB4 receptors phosphorylation ( activation ) and a relatively large decrease in intracellular levels of total and/or phosphorylated c-Raf, MEK1/2, ERK1/2, PI3K , PDK1, Akt, p-NF?B, Jak1, Jak2, and Stat1, as compared to cells treated with only one compound or in the vehicle treated control group
Yang et al., Journal of biomedical research 2011 : Furthermore, expression of dominant negative Rac1 ( T17N ) could largely block EGF induced PI3K/Akt-PAK1 activation and cell migration ... Interestingly, EGF could induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF induced ROS generation, cell migration, as well as activation of PI3K/Akt and PAK, but not Rac1
Lipson et al., J Pharmacol Exp Ther 1998 : A synthetic EGF receptor kinase inhibitor showed selective inhibitor properties when tested for EGF induced receptor autophosphorylation, MAPK activation, PI3K activation, entry into S phase and cyclin E-associated kinase activity
Wang et al., Cell Growth Differ 1998 : Serum and EGF induction of the core SRE was partially inhibited by rho and PI3K inhibitors