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Gene Review

EGFR  -  epidermal growth factor receptor

Homo sapiens

Synonyms: ERBB, ERBB1, Epidermal growth factor receptor, HER1, NISBD2, ...
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Disease relevance of EGFR

  • Here we provide evidence that prostaglandin E2 (PGE2) rapidly phosphorylates EGFR and triggers the extracellular signal-regulated kinase 2 (ERK2)--mitogenic signaling pathway in normal gastric epithelial (RGM1) and colon cancer (Caco-2, LoVo and HT-29) cell lines [1].
  • Our findings that PGE2 transactivates EGFR reveal a previously unknown mechanism by which PGE2 mediates trophic actions resulting in gastric and intestinal hypertrophy as well as growth of colonic polyps and cancers [1].
  • In two cell lines that overexpress erbB2 but do not expresss EGFR (MDA-MB-453 breast cancer cells and a Chinese hamster ovary cell line that had been transfected with erbB2), phosphorylation of p185erbB2 was induced only by gp30 [2].
  • Therefore, the EGFR retrovirus, which had a titer on NIH 3T3 cells that was greater than 10(7) focus-forming units per milliliter, can efficiently transfer and express this gene, and increased numbers of EGF receptors can contribute to the transformed phenotype [3].
  • Multivariate classification and regression-tree analysis of all 174 patients identified EGFR amplification as an independent predictor of prolonged survival in patients with glioblastoma multiforme who were older than 60 years of age [4].
  • Our results indicate that colorectal cancer cells may develop acquired resistance to cetuximab via altering EGFR levels through promotion of EGFR ubiquitination and degradation and using Src kinase-mediated cell signaling to bypass their dependency on EGFR for cell growth and survival [5].
  • Members of the miR-200 family appear to control the EMT process and sensitivity to EGFR therapy in bladder cancer cells and the expression of miR-200 is sufficient to restore EGFR dependency at least in some of the mesenchymal bladder cancer cells [6].
  • The possibility of differences in the mutational status of EGFR, KRAS, BRAF between primary tumors and corresponding lymph node metastases should be considered whenever these mutations are used for the selection of patients for EGFR-directed tyrosine kinase inhibitor therapy [7].
  • Strategies to optimize EGFR-targeted therapy in head and neck cancer involve not only the selection for patients most likely to benefit but also the use of combination therapies to target the network of pathways involved in tumor growth, invasion, angiogenesis, and metastasis [8].
  • In this review, we discuss recent advances in the understanding of acquired TKI resistance in EGFR-mutant lung cancer and review therapeutic progress with second generation TKIs and combinations of targeted therapies [9].
  • High-level EGFR amplification was rapidly lost in 5 glioblastoma cultures supplemented with EGF, whereas it was preserved in cultures from the same tumors established without EGF [10].

Psychiatry related information on EGFR


High impact information on EGFR

  • (2006) in this issue of Cell provides compelling evidence that the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) is activated by the formation of an asymmetric dimer, with one kinase domain in the EGF-mediated dimer activating the other through an allosteric mechanism [16].
  • We find that the EGFR kinase domain can be activated by increasing its local concentration or by mutating a leucine (L834R) in the activation loop, the phosphorylation of which is not required for activation [17].
  • The mechanism by which the epidermal growth factor receptor (EGFR) is activated upon dimerization has eluded definition [17].
  • Mathematical modeling of the EGF-EGFR binding kinetics measured at single molecule level using total internal reflectance fluorescence (TIRF) microcopy revealed that cells respond differently to the same concentration of EGF depending on the number of EGFRs expressed. Compared to the Hela cells (aproximately 50,000 receptors/cell), EGFR-overexpressing MDA-468 cells (>1 million receptors/cell) show; (a) higher number of pre-formed dimers, (b) improved EGF-EGFR interaction at lower ligand concentrations, and (c) shorter time-lapse between first and second EGF binding to the dimer [18] .
  • Treatment with a pharmacological inhibitor of EGFR, AG1478, dramatically increases the extent of pre-formed EGFR dimers [18].
  • These observations implicate altered EGFR signaling in genetic susceptibility to lung cancer [19].
  • Inherited susceptibility to lung cancer may be associated with the T790M drug resistance mutation in EGFR [19].

Chemical compound and disease context of EGFR


Biological context of EGFR


Anatomical context of EGFR


Associations of EGFR with chemical compounds

  • Inactivation of EGFR kinase with selective inhibitors significantly reduces PGE2-induced ERK2 activation, c-fos mRNA expression and cell proliferation [1].
  • By use of a colony-forming assay, the 1-hour IC50 (i.e., the concentration of drug required for 1 hour to achieve 50% cell kill) for cisplatin was 2 microM or less for parental and vector-transfected clones (n = 4), whereas it was 25 microM or more for all MDA-468/AS-EGFR clones (n = 3) [32].
  • We have identified a regulated interaction between parkin and Eps15, an adaptor protein that is involved in epidermal growth factor (EGF) receptor (EGFR) endocytosis and trafficking [33].
  • EGFR-dependent adhesion was noted when the ligands were tethered to inert beads, simulating the physiologically relevant presentation of tenascin-C as hexabrachion, and suggesting an increase in avidity similar to that seen for integrin ligands upon surface binding [34].
  • Transient expression of either Gq- or Gi-coupled receptors in COS-7 cells allowed GPCR agonist-induced EGFR transactivation, and lysophosphatidic acid (LPA)-generated signals involved the docking protein Gab1 [35].
  • Within this ordered complex of signaling molecules, the ability of CD82 to associate with PKC-alpha requires the presence of caveolin-1, whereas the interaction of caveolin-1 or PKC-alpha with EGFR requires the presence of CD82 and ganglioside GM3 [36].
  • Activation of TACE was dependent upon a discrete interaction between the previously defined IgG-binding domain of protein A and the epidermal growth factor receptor (EGFR), which in turn induced TACE phosphorylation through a c-Src-erk1/2-mediated cascade [37].
  • Taken together, these findings suggest that EGCG inhibits the binding of EGF to the EGFR and the subsequent dimerization and activation of the EGFR by altering membrane organization [38].
  • EGFR activation by menadione was associated with reversible protein tyrosine phosphatase inhibition, which seemed to be mediated by ROS generation as exposure to antioxidants prevented both menadione-induced ROS generation and phosphatase inhibition [39].
  • Afatinib (BIBW-2992), an irreversible kinase inhibitor targeting EGFR and HER2, successfully inhibited growth of the cetuximab-resistant cells in vitro [40].
  • EGFR protein expression using an ID-specific antibody specifically predicts response to gefitinib in NSCLC patients, including in EGFR-mutated patients, and increased PFS/OS from gefitinib [41].

Physical interactions of EGFR

  • Shc immunoprecipitates performed after IGF-1 stimulation contain coprecipitated EGFR, suggesting that IGF-1R activation induces the assembly of EGFR.Shc complexes [42].
  • We mapped the EGFR phosphotyrosine 1173 as the major binding site for SHP-1 by a combination of phosphopeptide activation, phosphopeptide competition, and receptor YF mutant analysis [43].
  • By gel filtration chromatography, we show that Ent-1 and SNX1 co-eluted in macromolecular complexes containing part of EGFR [44].
  • RGS16 co-immunoprecipitated with EGFR, and the interaction did not require EGFR activation [45].
  • Finally, the PKAI-EGF-R association occurs through the binding of RIalpha to the SH3 domain(s) of Grb2 adaptor protein, thus allowing the recruitment of the PKAI holoenzyme to the activated EGF-R [46].
  • Tyrosine-phosphorylated TLR4 interacts with EGFR [47].

Enzymatic interactions of EGFR

  • The protein-tyrosine phosphatase SHP-1 binds to and dephosphorylates the epidermal growth factor receptor (EGFR), and both SH2 domains of SHP-1 are important for this interaction (Tenev, T., Keilhack, H., Tomic, S., Stoyanov, B., Stein-Gerlach, M., Lammers, R., Krivtsov, A. V., Ullrich, A., and Böhmer, F. D. (1997) J. Biol. Chem. 272, 5966-5973) [43].
  • Purified EGFR phosphorylated only recombinant RGS16 wild-type or Y177F in vitro, implying that EGFR-mediated phosphorylation depended on residue Tyr(168) [45].
  • Combined cell lysates were affinity-purified over the SH2 domain of the adapter protein Grb2 (GST-SH2 fusion protein) that specifically binds phosphorylated EGFR and Src homologous and collagen (Shc) protein [48].
  • Dok-R has previously been shown to associate with the epidermal growth factor receptor (EGFR) and become tyrosine phosphorylated in response to EGF stimulation [49].
  • METHODS: Expression of EGFR and ligand-independent EGFRvIII mutant proteins and of phosphorylated protein kinase B (PKB)/Akt in specimens from glioma patients were assessed by immunohistochemistry [50].

Co-localisations of EGFR

  • Moreover, activated endogenous epidermal growth factor receptor (EGFR) colocalizes markedly with SNX2-positive endosomes, but minimally with SNX1-containing vesicles [51].
  • Grb2 and the EGFR are internalized and co-localized in endocytic vesicles in response to EGF [52].
  • Furthermore, EGFR colocalized with IP receptor in the glandular epithelial compartment [53].
  • The dexamethasone-induced block of Grb2 recruitment was parallelled by changes in phosphorylation status and subcellular localization of lipocortin 1 (LC1) and an increase in the amount of the tyrosine phosphoprotein co-localized with EGF-R [54].
  • We also demonstrated up-regulated caveolin proteins were co-localized with EGFR proteins in detergent-insoluble fractions [55].

Regulatory relationships of EGFR


Other interactions of EGFR

  • PTEN mutation, EGFR amplification, and outcome in patients with anaplastic astrocytoma and glioblastoma multiforme [4].
  • TxB regulation of EGFR-ERK1/2 signaling pathways was determined using immunoblot analysis, confocal microscopy, and enzyme-linked immunosorbent assay, whereas IL-8 gene expression was measured by luciferase promoter assay [62].
  • Interestingly, DT-induced 22Na+ influx was weak in DTR-EGFR cells and not detectable in DTR-GPI cells [63].
  • Furthermore, we have identified a short sequence motif (YV/IN) present in IRS-1, EGFR and Shc, which specifically binds the SH2 domain of GRB2 with high affinity [64].
  • The transmission of mitogenic signal induced by EGF-EGFR interaction is mediated via activation of nuclear factor kappaB (NF-kappaB) [56].
  • These results identify a novel mediator of the EGFR transcription function and further suggest that nuclear EGFR and the lipid kinase PIKfyve may play a role in bladder oncogenesis [65].
  • Overexpression of dominant negative Rab5a or depletion of all three isoforms of Rab5 does not inhibit ubiquitination of EGFR, which suggests that GAPex-5-mediated EGFR ubiquitination is independent of Rab5 activation [66].
  • In separate multivariate analyses that adjusted for the effects of standard preoperative predictors, lower EGFR, higher HER2, and higher HER2/EGFR ratio were associated with prostate-specific antigen (PSA) progression (P = 0.003, P < 0.001, and P < 0.001, respectively) [67].
  • These results indicate that HER2 affects glial-cell migration by modulating EGFR-HER2 signal transduction, and that this effect is mediated by N-cadherin [68].
  • These results implicate TACE as a promising target of EGFR axis inhibition in CRC [69].
  • TGF-β treatment in EGFR targeted knock-down cells correlates with higher levels of the NADPH oxidase NOX4 and changes in the expression profile of BCL-2 and IAP families [70].

Analytical, diagnostic and therapeutic context of EGFR


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  2. Direct interaction of a ligand for the erbB2 oncogene product with the EGF receptor and p185erbB2. Lupu, R., Colomer, R., Zugmaier, G., Sarup, J., Shepard, M., Slamon, D., Lippman, M.E. Science (1990) [Pubmed]
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  6. miR-200 expression regulates epithelial-to-mesenchymal transition in bladder cancer cells and reverses resistance to epidermal growth factor receptor therapy. Adam, L., Zhong, M., Choi, W., Qi, W., Nicoloso, M., Arora, A., Calin, G., Wang, H., Siefker-Radtke, A., McConkey, D., Bar-Eli, M., Dinney, C. Clin. Cancer Res. (2009) [Pubmed]
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  15. Conditioned place preference and locomotor sensitization after repeated administration of cocaine or methamphetamine in rats treated with epidermal growth factor during the neonatal period. Mizuno, M., Malta, R.S., Nagano, T., Nawa, H. Ann. N. Y. Acad. Sci. (2004) [Pubmed]
  16. EGF receptor activation: push comes to shove. Hubbard, S.R. Cell (2006) [Pubmed]
  17. An allosteric mechanism for activation of the kinase domain of epidermal growth factor receptor. Zhang, X., Gureasko, J., Shen, K., Cole, P.A., Kuriyan, J. Cell (2006) [Pubmed]
  18. Receptor overexpression or inhibition alters cell surface dynamics of EGF-EGFR interaction: new insights from real-time single molecule analysis. Yu, C., Hale, J., Ritchie, K., Prasad, N.K., Irudayaraj, J. Biochem. Biophys. Res. Commun. (2009) [Pubmed]
  19. Inherited susceptibility to lung cancer may be associated with the T790M drug resistance mutation in EGFR. Bell, D.W., Gore, I., Okimoto, R.A., Godin-Heymann, N., Sordella, R., Mulloy, R., Sharma, S.V., Brannigan, B.W., Mohapatra, G., Settleman, J., Haber, D.A. Nat. Genet. (2005) [Pubmed]
  20. Blocking airway mucous cell metaplasia by inhibiting EGFR antiapoptosis and IL-13 transdifferentiation signals. Tyner, J.W., Kim, E.Y., Ide, K., Pelletier, M.R., Roswit, W.T., Morton, J.D., Battaile, J.T., Patel, A.C., Patterson, G.A., Castro, M., Spoor, M.S., You, Y., Brody, S.L., Holtzman, M.J. J. Clin. Invest. (2006) [Pubmed]
  21. A novel acylglycerol kinase that produces lysophosphatidic acid modulates cross talk with EGFR in prostate cancer cells. Bektas, M., Payne, S.G., Liu, H., Goparaju, S., Milstien, S., Spiegel, S. J. Cell Biol. (2005) [Pubmed]
  22. ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines. Engelman, J.A., Jänne, P.A., Mermel, C., Pearlberg, J., Mukohara, T., Fleet, C., Cichowski, K., Johnson, B.E., Cantley, L.C. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  23. Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib. Kwak, E.L., Sordella, R., Bell, D.W., Godin-Heymann, N., Okimoto, R.A., Brannigan, B.W., Harris, P.L., Driscoll, D.R., Fidias, P., Lynch, T.J., Rabindran, S.K., McGinnis, J.P., Wissner, A., Sharma, S.V., Isselbacher, K.J., Settleman, J., Haber, D.A. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  24. Intron 1 CA dinucleotide repeat polymorphism and mutations of epidermal growth factor receptor and gefitinib responsiveness in non-small-cell lung cancer. Han, S.W., Jeon, Y.K., Lee, K.H., Keam, B., Hwang, P.G., Oh, D.Y., Lee, S.H., Kim, D.W., Im, S.A., Chung, D.H., Heo, D.S., Bang, Y.J., Kim, T.Y. Pharmacogenet. Genomics (2007) [Pubmed]
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  26. Overexpression of the human EGF receptor confers an EGF-dependent transformed phenotype to NIH 3T3 cells. Di Fiore, P.P., Pierce, J.H., Fleming, T.P., Hazan, R., Ullrich, A., King, C.R., Schlessinger, J., Aaronson, S.A. Cell (1987) [Pubmed]
  27. EGF receptor signaling stimulates SRC kinase phosphorylation of clathrin, influencing clathrin redistribution and EGF uptake. Wilde, A., Beattie, E.C., Lem, L., Riethof, D.A., Liu, S.H., Mobley, W.C., Soriano, P., Brodsky, F.M. Cell (1999) [Pubmed]
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  29. Chimeric NGF-EGF receptors define domains responsible for neuronal differentiation. Yan, H., Schlessinger, J., Chao, M.V. Science (1991) [Pubmed]
  30. Reduced epidermal growth factor receptor expression in hypohidrotic ectodermal dysplasia and Tabby mice. Vargas, G.A., Fantino, E., George-Nascimento, C., Gargus, J.J., Haigler, H.T. J. Clin. Invest. (1996) [Pubmed]
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  33. A regulated interaction with the UIM protein Eps15 implicates parkin in EGF receptor trafficking and PI(3)K-Akt signalling. Fallon, L., Bélanger, C.M., Corera, A.T., Kontogiannea, M., Regan-Klapisz, E., Moreau, F., Voortman, J., Haber, M., Rouleau, G., Thorarinsdottir, T., Brice, A., van Bergen En Henegouwen, P.M., Fon, E.A. Nat. Cell Biol. (2006) [Pubmed]
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  36. Suppression of epidermal growth factor receptor signaling by protein kinase C-alpha activation requires CD82, caveolin-1, and ganglioside. Wang, X.Q., Yan, Q., Sun, P., Liu, J.W., Go, L., McDaniel, S.M., Paller, A.S. Cancer Res. (2007) [Pubmed]
  37. Staphylococcus aureus protein A activates TACE through EGFR-dependent signaling. Gómez, M.I., Seaghdha, M.O., Prince, A.S. EMBO J. (2007) [Pubmed]
  38. The inhibitory effect of (-)-epigallocatechin gallate on activation of the epidermal growth factor receptor is associated with altered lipid order in HT29 colon cancer cells. Adachi, S., Nagao, T., Ingolfsson, H.I., Maxfield, F.R., Andersen, O.S., Kopelovich, L., Weinstein, I.B. Cancer Res. (2007) [Pubmed]
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