ArticleNature medicine2017
Cytoplasmic p53 couples oncogene-driven glucose metabolism to apoptosis and is a therapeutic target in glioblastoma.
Article in Nature medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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Who cites it
69 citing papers in PubMed, 102 citations in OpenAlex.
- Emerging roles of ferroptosis in modulating the immune landscape of glial tumours.Nature cell biology · 2026Review
- Identification of glycometabolism-related genes for predicting the prognosis of patients with glioblastoma and its correlation with immune infiltration.Discover oncology · 2026Article
- Ependymoma group-specific blood-brain barrier differences uncovered by a multi-omics approach.Scientific reports · 2026Article
- Metabolism-related ALDH1B1 acts as potential predictor and therapeutic target for primary gastrointestinal diffuse large B-cell lymphoma.Apoptosis : an international journal on programmed cell death · 2025Article
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Harnessing p53 for targeted cancer therapy: new advances and future directions.Transcription · 2025Review
- Advances in Synthetic Lethality in Potential Oncology Therapeutic Approaches.Current topics in medicinal chemistry · 2025Review
- Ferroptosis-related gene signature-based subtype identification of triple-negative breast cancer to prioritize treatment strategies.Frontiers in oncology · 2025Article
- Integrated molecular and functional characterization of the intrinsic apoptotic machinery identifies therapeutic vulnerabilities in glioma.Nature communications · 2024Article
- Tumor Microenvironment-Responsive Nanocapsule Delivery CRISPR/Cas9 to Reprogram the Immunosuppressive Microenvironment in Hepatoma Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- CDK7 and CDK9 inhibition interferes with transcription, translation, and stemness, and induces cytotoxicity in GBM irrespective of temozolomide sensitivity.Neuro-oncology · 2024Article
- A cytosolic mutp53(E285K) variant confers chemoresistance of malignant melanoma.Cell death & disease · 2023Article
- Glioblastomas: Hijacking Metabolism to Build a Flexible Shield for Therapy Resistance.Antioxidants & redox signaling · 2023Review
- Article
- Silencing GMPPB Inhibits the Proliferation and Invasion of GBM via Hippo/MMP3 Pathways.International journal of molecular sciences · 2023Article
- The Spectrum of Molecular Pathways in Gliomas-An Up-to-Date Review.Biomedicines · 2023Review
- Article
- Early Reduction of Glucose Consumption Is a Biomarker of Kinase Inhibitor Efficacy Which Can Be Reversed with GLUT1 Overexpression in Lung Cancer Cells.Molecular imaging and biology · 2023Article
- Metabolic Rewiring in Adult-Type Diffuse Gliomas.International journal of molecular sciences · 2023Review
- The ARTS of p53-dependent mitochondrial apoptosis.Journal of molecular cell biology · 2023Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
Cross-talk among oncogenic signaling and metabolic pathways may create opportunities for new therapeutic strategies in cancer. Here we show that although acute inhibition of EGFR-driven glucose metabolism induces only minimal cell death, it lowers the apoptotic threshold in a subset of patient-derived glioblastoma (GBM) cells. Mechanistic studies revealed that after attenuated glucose consumption, Bcl-xL blocks cytoplasmic p53 from triggering intrinsic apoptosis. Consequently, targeting of EGFR-driven glucose metabolism in combination with pharmacological stabilization of p53 with the brain-penetrant small molecule idasanutlin resulted in synthetic lethality in orthotopic glioblastoma xenograft models. Notably, neither the degree of EGFR-signaling inhibition nor genetic analysis of EGFR was sufficient to predict sensitivity to this therapeutic combination. However, detection of rapid inhibitory effects on [
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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.