ArticleCancer letters2010
EGFR and EGFRvIII interact with PUMA to inhibit mitochondrial translocalization of PUMA and PUMA-mediated apoptosis independent of EGFR kinase activity.
Article in Cancer letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 59 citations in OpenAlex.
- Cut the fat: targeting cholesterol and lipid metabolism in glioblastoma.Cell death & disease · 2025Review
- A PROTAC degrader suppresses oncogenic functions of PTK6, inducing apoptosis of breast cancer cells.Cell chemical biology · 2025Article
- Targeting Epidermal Growth Factor Receptor for Cancer Treatment: Abolishing Both Kinase-Dependent and Kinase-Independent Functions of the Receptor.Pharmacological reviews · 2023Review
- OTUD7B Activates Wnt Signaling Pathway through the Interaction with LEF1.Biomolecules · 2023Article
- Article
- Fluorescence Imaging of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance in Non-Small Cell Lung Cancer.Cancers · 2022Review
- Novel Tyrosine Kinase Targets in Urothelial Carcinoma.International journal of molecular sciences · 2021Review
- Kinase-Inactivated EGFR Is Required for the Survival of Wild-Type EGFR-Expressing Cancer Cells Treated with Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2019Article
- Rethink of EGFR in Cancer With Its Kinase Independent Function on Board.Frontiers in oncology · 2019Article
- Sym004-induced EGFR elimination is associated with profound anti-tumor activity in EGFRvIII patient-derived glioblastoma models.Journal of neuro-oncology · 2018Article
- FHL2 interacts with EGFR to promote glioblastoma growth.Oncogene · 2018Article
- Emerging functions of the EGFR in cancer.Molecular oncology · 2018Review
- Non-kinase targets of protein kinase inhibitors.Nature reviews. Drug discovery · 2017Review
- Differential protein stability of EGFR mutants determines responsiveness to tyrosine kinase inhibitors.Oncotarget · 2016Article
- Cell line with endogenous EGFRvIII expression is a suitable model for research and drug development purposes.Oncotarget · 2016Article
- Stress-Induced EGFR Trafficking: Mechanisms, Functions, and Therapeutic Implications.Trends in cell biology · 2016Review
- How to train glioma cells to die: molecular challenges in cell death.Journal of neuro-oncology · 2016Article
- EGFR and HER2 signaling in breast cancer brain metastasis.Frontiers in bioscience (Elite edition) · 2016Article
- Tetrathiomolybdate mediates cisplatin-induced p38 signaling and EGFR degradation and enhances response to cisplatin therapy in gynecologic cancers.Scientific reports · 2015Article
- Subcellular localization of PUMA regulates its pro-apoptotic activity in Burkitt's lymphoma B cells.Oncotarget · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
EGFR and its constitutively activated variant EGFRvIII are linked to glioblastoma resistance to therapy, the mechanisms underlying this association, however, are still unclear. We report that in glioblastoma, EGFR/EGFRvIII paradoxically co-expresses with p53-upregulated modulator of apoptosis (PUMA), a proapoptotic member of the Bcl-2 family of proteins primarily located on the mitochondria. EGFR/EGFRvIII binds to PUMA constitutively and under apoptotic stress, and subsequently sequesters PUMA in the cytoplasm. The EGFR-PUMA interaction is independent of EGFR activation and is sustained under EGFR inhibition. A Bcl-2/Bcl-xL inhibitor that mimics PUMA activity sensitizes EGFR/EGFRvIII-expressing glioblastoma cells to Iressa. Collectively, we uncovered a novel kinase-independent function of EGFR/EGFRvIII that leads to tumor drug resistance.
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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.