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CDH1 — EGFR

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: MAPK3 → Complex of CDH1-EGFR (increases, CDH1/EGFR Activity)
  Evidence: In human HaCaT keratinocytes for instance, ERK1/2 phosphorylation increases in dependence of EGF-R recruitment to transadhering E-cadherin, and E-cadherin-mediated activation of MAPK was also reported in intestinal epithelial cells (Pece and Gutkind, 2000; Laprise et al., 2004).
• OpenBEL Selventa BEL large corpus: Complex of CDH1-EGFR → EGFR (directlyIncreases)
  Evidence: Western blot analysis with anti-E-cadherin antibody showed that the amount of E-cadherin beta-catenin complexes was substantially reduced (57%) in EGFR anti-sense vector-expressing NIH:OVCAR-8 cells (Fig. 8a[1]). Similarly, complexes between alpha-catenin and E-cadherin were absent in EGFR anti-sense vector-transfected NIH:OVCAR-8 cells (Fig. 8a[2]). In these cells, the amount of E-cadherin was reduced 40% when compared to control cells (Fig. 8a[3]). As expected, levels of E-cadherin complexed t...
• NCI Pathway Database Posttranslational regulation of adherens junction stability and dissassembly: EGFR/EGFR/EGF/EGF complex (EGFR-EGF) → E-cadherin/Ca2+/beta catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1-CTNNA1-CTNND1) (modification, activates)
  Miravet et al., Mol Cell Biol 2003, Hoschuetzky et al., J Cell Biol 1994, Shibamoto et al., Cell adhesion and communication 1994
  Evidence: assay, physical interaction
• NCI Pathway Database Stabilization and expansion of the E-cadherin adherens junction: EGFR (EGFR) → E-cadherin/Ca2+/beta catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1-CTNNA1-CTNND1) (modification, collaborate)
  Qian et al., EMBO J 2004, Hoschuetzky et al., J Cell Biol 1994, Takahashi et al., Exp Cell Res 1996
  Evidence: assay, physical interaction
• NCI Pathway Database Stabilization and expansion of the E-cadherin adherens junction: E-cadherin/Ca2+/beta catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1-CTNNA1-CTNND1) → EGFR/EGFR/EGF/EGF complex (EGFR-EGF) (modification, inhibits)
  Qian et al., EMBO J 2004, Hoschuetzky et al., J Cell Biol 1994, Takahashi et al., Exp Cell Res 1996
  Evidence: assay, physical interaction
• NCI Pathway Database E-cadherin signaling in keratinocytes: EGFR (EGFR) → E-cadherin/Ca2+/beta catenin-gamma catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1_JUP-CTNNA1-CTNND1) (modification, collaborate)
  Pece et al., J Biol Chem 2000, Betson et al., J Biol Chem 2002
  Evidence: assay, physical interaction
• NCI Pathway Database E-cadherin signaling in keratinocytes: E-cadherin/Ca2+/beta catenin-gamma catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1_JUP-CTNNA1-CTNND1) → EGFR(dimer) complex (EGFR) (modification, activates)
  Pece et al., J Biol Chem 2000, Betson et al., J Biol Chem 2002
  Evidence: assay, physical interaction

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Bind Interaction: CDH1 — EGFR Fedor-Chaiken et al., Cell communication & adhesion 2003*
• IRef Bind_translation Interaction: CDH1 — EGFR (imaging technique) Fedor-Chaiken et al., Cell communication & adhesion 2003*
• IRef Bind_translation Interaction: CDH1 — EGFR (coimmunoprecipitation) Fedor-Chaiken et al., Cell communication & adhesion 2003*
• IRef Biogrid Interaction: CDH1 — EGFR (physical association, affinity chromatography technology) Pece et al., J Biol Chem 2000
• IRef Hprd Interaction: EGFR — CDH1 (in vivo) Pece et al., J Biol Chem 2000
• IRef Innatedb Interaction: CDH1 — EGFR (unknown, -) Heijink et al., J Immunol 2007*
• IRef Intact Interaction: Complex of 59 proteins (association, tandem affinity purification) Li et al., Molecular systems biology 2013
• IRef Intact Interaction: Complex of 24 proteins (association, tandem affinity purification) Li et al., Molecular systems biology 2013
• IRef Ophid Interaction: CDH1 — EGFR (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Andl et al., J Biol Chem 2003 : In particular, EGFR induced effects upon aggregation appear to be mediated through the relocalization of p120 from the cytoplasm to the membrane and increased interaction with E-cadherin
Fedor-Chaiken et al., Cell communication & adhesion 2003 (Breast Neoplasms...) : We found that E-cadherin and epidermal growth factor receptor (EGFR) are associated in mammary epithelial cells and that E-cadherin engagement in these cells induces transient activation of EGFR, as previously seen in keratinocytes ( 37 )
Qian et al., EMBO J 2004 : EGFR regulation by E-cadherin was associated with complex formation between EGFR and E-cadherin that depended on the extracellular domain of E-cadherin but was independent of beta-catenin binding or p120-catenin binding
Reddy et al., Mol Endocrinol 2005 (MAP Kinase Signaling System...) : Akt activation is mediated through the activation of phosphatidylinositol 3 kinase, and both Akt and MAPK activation are mediated by an E-cadherin adhesion induced ligand independent activation of epidermal growth factor receptor
Kim et al., Am J Physiol Lung Cell Mol Physiol 2005 : E-cadherin blockade also increased EGFR dependent cell proliferation and TGF-alpha induced EGFR tyrosine phosphorylation in dense cultures of NCI-H292 cells, suggesting that E-cadherin promotes EGFR dependent mucin production and inhibits EGFR dependent cell proliferation via modulation of EGFR phosphotyrosine levels
Lin et al., FEBS Lett 2006 (Carcinoma, Hepatocellular...) : Furthermore, inhibition of the epidermal growth factor receptor (EGFR) with gefitinib partially prevented the downregulation of E-cadherin and beta-catenin at the adherens junctions and migration behavior induced by RAW/AMCM
Perrais et al., Mol Biol Cell 2007 : E-cadherin homophilic ligation inhibits cell growth and epidermal growth factor receptor signaling independently of other cell interactions ... E-cadherin ligation also inhibits epidermal growth factor (EGF) receptor mediated growth signaling by a beta-catenin dependent mechanism
Yates et al., Br J Cancer 2007 (Prostatic Neoplasms) : Inhibition of autocrine EGFR signalling increased E-cadherin expression and cell-cell heterotypic adhesion ; further, expression of a downregulation-resistant EGFR variant prevented E-cadherin upregulation
Mateus et al., Hum Mol Genet 2007 : Furthermore, we demonstrate that E-cadherin dependent EGFR activation contributes to enhanced cell motility, in a mechanism involving RhoA activation
Heijink et al., J Immunol 2007 (Asthma) : Small interference RNA silencing of E-cadherin resulted in loss of E-cadherin mediated junctions, enhanced phosphorylation of epidermal growth factor receptor (EGFR) , and the downstream targets MEK/ERK-1/2 and p38 MAPK, finally resulting in up-regulation of TARC as well as thymic stromal lymphopoietin expression
O'Keefe et al., Dev Biol 2007 : Egfr/Ras signaling regulates DE-cadherin/Shotgun localization to control vein morphogenesis in the Drosophila wing
Shen et al., J Biol Chem 2008 : Silencing Cdc42 blocks activation of EGFR and Src induced by Ca2+ depletion, resulting in a reduction in E-cadherin degradation
Bremm et al., Cancer Res 2008 (Breast Neoplasms...) : In summary, we describe activation of EGFR by mutant E-cadherin as a novel mechanism in tumor cells that explains the enhanced motility of tumor cells in the presence of an extracellular mutation of E-cadherin
Cowden Dahl et al., Cancer Res 2008 (Neoplasm Invasiveness...) : Epidermal growth factor (EGF) receptor ( EGFR ) is frequently elevated in epithelial ovarian cancer, and E-cadherin expression is often reduced in advanced disease
Klessner et al., Mol Biol Cell 2009 : We previously showed that EGFR inhibition results in accumulation of the desmosomal cadherin , desmoglein 2 (Dsg2), at cell-cell interfaces accompanied by inhibition of matrix metalloprotease ( MMP ) -dependent shedding of the Dsg2 ectodomain and tyrosine phosphorylation of its cytoplasmic domain
Rieber et al., Int J Cancer 2009 (Breast Neoplasms...) : Since the p53 tumor suppressor pathway is inactivated in most human cancers due to gene mutations or defective wt p53 signaling, we now investigated in human wt p53 breast carcinoma MCF-7 cells, whether single treatment with the p53 transactivation pharmacological inhibitor pifithrin-alpha, transient p53 siRNA interference or stable insertion of a dominant negative ( DN ) R175H p53 mutant increase : ( i ) EGFR/erbB1 activation , ( ii ) MMP-9 expression and ( iii ) loss of surface E-cadherin
Gan et al., Oncogene 2010 (MAP Kinase Signaling System...) : Knockdown of endogenous Snail also prevents EGFR mediated downregulation of E-cadherin , EMT and cell migration ... Knockdown of endogenous Snail also prevents EGFR mediated downregulation of E-cadherin , EMT and cell migration
Cheng et al., Mol Endocrinol 2010 (Ovarian Neoplasms) : In ovarian cancer, it has been shown that E-cadherin is down-regulated by epidermal growth factor (EGF) receptor ( EGFR ) activation, and that cells with low E-cadherin expression are particularly invasive
Black et al., J Urol 2011 (Disease Models, Animal...) : Inhibition of epidermal growth factor receptor and platelet derived growth factor receptor-ß receptors blocked cell invasion, decreased cell proliferation, reduced xenograft tumor growth and increased E-cadherin expression
Sorscher et al., Biochem Biophys Res Commun 1995 : These results suggest that EGFr activation may regulate or enhance E-cadherin expression