ArticleOncogene2015
EGFR wild type antagonizes EGFRvIII-mediated activation of Met in glioblastoma.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- The glioblastoma ecosystem: clonal evolution, heterogeneity, and therapeutic resistance.Frontiers in cell and developmental biology · 2026Review
- Polymeric Nanoparticle-Mediated Photodynamic Therapy: A Synergistic Approach for Glioblastoma Treatment.Pharmaceuticals (Basel, Switzerland) · 2025Review
- LncRNA APTR amplification serves as a potential glioma biomarker and promotes glioma progression via miR-6734-5p/ TCF7/LEF1 axis.Non-coding RNA research · 2025Article
- EGFRvIII Confers Sensitivity to Saracatinib in a STAT5-Dependent Manner in Glioblastoma.International journal of molecular sciences · 2024Article
- Targeting RTK-PI3K-mTOR Axis in Gliomas: An Update.International journal of molecular sciences · 2021Review
- Poly(p-phenylenevinylene) nanoparticles modified with antiEGFRvIII for specific glioblastoma therapy.Scientific reports · 2021Article
- ERK-mediated negative feedback regulation of oncogenic EGFRvIII in glioblastoma cells.Oncology letters · 2020Article
- EGFR-vIII downregulated H2AZK4/7AC though the PI3K/AKT-HDAC2 axis to regulate cell cycle progression.Clinical and translational medicine · 2020Article
- HeterogeneousCancers · 2020Article
- Functional RNAi Screens Define Distinct Protein Kinase Vulnerabilities in EGFR-Dependent HNSCC Cell Lines.Molecular pharmacology · 2019Article
- MET in glioma: signaling pathways and targeted therapies.Journal of experimental & clinical cancer research : CR · 2019Review
- The third-generation EGFR inhibitor AZD9291 overcomes primary resistance by continuously blocking ERK signaling in glioblastoma.Journal of experimental & clinical cancer research : CR · 2019Article
- The RTK Interactome: Overview and Perspective on RTK Heterointeractions.Chemical reviews · 2019Review
- Cancer-Associated Fibroblasts Drive Glycolysis in a Targetable Signaling Loop Implicated in Head and Neck Squamous Cell Carcinoma Progression.Cancer research · 2018Article
- Correlation analysis of mesenchymal-epithelial transition factor protein and human epidermal growth receptor 2 protein expression in 1479 cases of lung adenocarcinoma in China.Thoracic cancer · 2018Article
- Epidermal growth factor receptor and EGFRvIII in glioblastoma: signaling pathways and targeted therapies.Oncogene · 2018Review
- FHL2 interacts with EGFR to promote glioblastoma growth.Oncogene · 2018Article
- CyclicOncotarget · 2018Article
- Multiplexed Exchange-PAINT imaging reveals ligand-dependent EGFR and Met interactions in the plasma membrane.Scientific reports · 2017Article
- Temozolomide induces autophagy in primary and established glioblastoma cells in an EGFR independent manner.Oncology letters · 2017Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Epidermal growth factor receptor (EGFR)vIII is the most common EGFR mutant found in glioblastoma (GBM). EGFRvIII does not bind ligand, is highly oncogenic and is usually coexpressed with EGFR wild type (EGFRwt). EGFRvIII activates Met, and Met contributes to EGFRvIII-mediated oncogenicity and resistance to treatment. Here, we report that addition of EGF results in a rapid loss of EGFRvIII-driven Met phosphorylation in glioma cells. Met is associated with EGFRvIII in a physical complex. Addition of EGF results in a dissociation of the EGFRvIII-Met complex with a concomitant loss of Met phosphorylation. Consistent with the abrogation of Met activation, addition of EGF results in the inhibition of EGFRvIII-mediated resistance to chemotherapy. Thus, our study suggests that ligand in the milieu of EGFRvIII-expressing GBM cells is likely to influence the EGFRvIII-Met interaction and resistance to treatment, and highlights a novel antagonistic interaction between EGFRwt and EGFRvIII in glioma cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.