ArticleThe Journal of biological chemistry2013
Access to the nucleus and functional association with c-Myc is required for the full oncogenic potential of ΔEGFR/EGFRvIII.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
13 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Nuclear epidermal growth factor receptor as a therapeutic target.Exploration of targeted anti-tumor therapy · 2023Review
- Nuclear export signal mutation of epidermal growth factor receptor enhances malignant phenotypes of cancer cells.American journal of cancer research · 2023Article
- Syngeneic murine glioblastoma models: reactionary immune changes and immunotherapy intervention outcomes.Neurosurgical focus · 2022Article
- Shuttling of cellular proteins between the plasma membrane and nucleus (Review).Molecular medicine reports · 2022Review
- EGFRvIII Promotes Cell Survival during Endoplasmic Reticulum Stress through a Reticulocalbin 1-Dependent Mechanism.Cancers · 2021Article
- EGFRJournal of oncology · 2019Review
- COPI-Mediated Nuclear Translocation of EGFRvIII Promotes STAT3 Phosphorylation and PKM2 Nuclear Localization.International journal of biological sciences · 2019Article
- Finding the Right Way to Target EGFR in Glioblastomas; Lessons from Lung Adenocarcinomas.Cancers · 2018Article
- RETRACTED: The receptor tyrosine kinase AXL mediates nuclear translocation of the epidermal growth factor receptor.Science signaling · 2017Article
- Non-canonical signaling mode of the epidermal growth factor receptor family.American journal of cancer research · 2015Review
- Nuclear epidermal growth factor receptor is a functional molecular target in triple-negative breast cancer.Molecular cancer therapeutics · 2014Article
- Immunocompetent murine models for the study of glioblastoma immunotherapy.Journal of translational medicine · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
ΔEGFR is a potent glioblastoma oncogene which has been studied primarily as a plasma membrane kinase. Using intracranial xenograft studies in mice, we show that blocking ΔEGFR access to the nucleus attenuates its tumorigenicity and, conversely, that promoting nuclear accumulation enhances this, providing the first in vivo evidence that the nuclear actions of ΔEGFR contribute strongly to its oncogenic function. Nuclear actions of ΔEGFR include regulation of gene expression by participation in chromatin-bound complexes, and genome-wide mapping of these sequences by chromatin immunoprecipitation and massively parallel sequencing identified 2294 peaks. Bioinformatic analysis showed enrichment of the E-box motif in the dataset, and c-Myc and ΔEGFR were corecruited to the promoters of and transcriptionally activated a subset of nuclear ΔEGFR chromatin targets. Knockdown of c-Myc decreased the expression of these targets and diminished ΔEGFR-stimulated anchorage-independent colony formation. We conclude that transcriptional regulation of target genes by association with gene regulatory chromatin in cooperation with c-Myc by nuclear ΔEGFR makes a unique contribution to its oncogenicity and propose that this venue provides new targets for therapeutic intervention.
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What OpenQuestion holds
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.