ArticleNature cell biology2018
AMP kinase promotes glioblastoma bioenergetics and tumour growth.
Article in Nature cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 98 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
98 citing papers in PubMed, 160 citations in OpenAlex.
- AMPK Pathway Activation Markers in GBM: Expression Patterns and Clinical Associations in a Real-World Study.International journal of molecular sciences · 2026Article
- The dual role of AMPK in cancer metabolic reprogramming.Molecular biology reports · 2026Review
- AMPK Therapy-A Little Goes A Long Way.Cells · 2026Review
- Dual-responsive peptide nanoplatform for improved lung cancer therapy via the synergistic suppression of autophagy and drug efflux.Materials today. Bio · 2026Article
- The structural requirements of 3,5-substituted oxindoles that determine selective AMPK or GSK3β inhibition.RSC medicinal chemistry · 2026Article
- A novel multiplex RNAi therapy simultaneously targets Hif1a and Hif2a to defy retinal degeneration in two models of AMD.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Metabolic remodeling and immune evasion in glioblastoma: a focus on serine and lipid networks.Frontiers in oncology · 2026Review
- AMPK Limits MNNG-Induced Parthanatos by Inhibiting BH3-Only Protein Bim.International journal of molecular sciences · 2025Article
- CaMKK2 as a therapeutic target to combat metastasis in glioblastoma.Molecular biology reports · 2025Review
- TRIM65 regulates glucose metabolic reprogramming to promote glioma cell proliferation via ubiquitination and degradation of AMPK.NPJ precision oncology · 2025Article
- AMP-activated protein kinase mediates adaptation of glioblastoma cells to conditions of the tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2025Article
- Article
- Rethinking AMPK: A Reversible Switch Fortifying Cancer Cell Stress-Resilience.The Yale journal of biology and medicine · 2025Review
- Sodium nitrite orchestrates macrophage mimicry of tongue squamous carcinoma cells to drive lymphatic metastasis.British journal of cancer · 2025Article
- Small Molecule Modulators of AMP-Activated Protein Kinase (AMPK) Activity and Their Potential in Cancer Therapy.Journal of medicinal chemistry · 2025Review
- Deletion of AMP-activated protein kinase impairs metastasis and is rescued by ROS scavenging or ectopic CD36 expression.Cell reports · 2025Article
- Targeting protein synthesis pathways in MYC-amplified medulloblastoma.Discover oncology · 2025Review
- ASPHD1 Is a tumor-suppressive and prognostic marker in glioma.Frontiers in oncology · 2025Article
- Physical activity and glioblastoma: a paradigm shift in neuro-oncology therapy.Frontiers in oncology · 2025Review
- Exploring glioma heterogeneity through omics networks: from gene network discovery to causal insights and patient stratification.BioData mining · 2024Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
- Erratum issued
Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
Abstract
Stress is integral to tumour evolution, and cancer cell survival depends on stress management. We found that cancer-associated stress chronically activates the bioenergetic sensor AMP kinase (AMPK) and, to survive, tumour cells hijack an AMPK-regulated stress response pathway conserved in normal cells. Analysis of The Cancer Genome Atlas data revealed that AMPK isoforms are highly expressed in the lethal human cancer glioblastoma (GBM). We show that AMPK inhibition reduces viability of patient-derived GBM stem cells (GSCs) and tumours. In stressed (exercised) skeletal muscle, AMPK is activated to cooperate with CREB1 (cAMP response element binding protein-1) and promote glucose metabolism. We demonstrate that oncogenic stress chronically activates AMPK in GSCs that coopt the AMPK-CREB1 pathway to coordinate tumour bioenergetics through the transcription factors HIF1α and GABPA. Finally, we show that adult mice tolerate systemic deletion of AMPK, supporting the use of AMPK pharmacological inhibitors in the treatment of GBM.
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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.