ReviewFrontiers in cell and developmental biology2025
Targeting metabolic reprogramming in glioblastoma as a new strategy to overcome therapy resistance.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The trial behind it
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Who cites it
28 citing papers in PubMed.
- PLOD1 Catalytic Activity Stabilizes ENO1 by Limiting FBXW7-dependent Degradation to Promote Glycolysis and TMZ Resistance in Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Deciphering LonP1's role in glioblastoma: an alternative mechanism of treatment resistance.American journal of physiology. Cell physiology · 2026Article
- TRIM47 promotes cell viability, cell cycle progression, metabolic reprogramming, and inhibits apoptosis of glioma via the NF-κB signaling pathway.Translational cancer research · 2026Article
- Clinical Applications of Hyperpolarized Magnetic Resonance Imaging in Brain Tumors: Current Evidence and Future Opportunities.Cancers · 2026Review
- AS1411-Induced Lipidomic Alterations and Therapeutic Insights in U-87 Glioblastoma Cells.Biomolecules · 2026Article
- Amino-acids-mTORC1-driven DDA1 phosphorylation promotes DNA repair and glioblastoma progression.Cell communication and signaling : CCS · 2026Article
- FABP7: A Regulator of Neuro-Immune Metabolic Networks and Therapeutic Vulnerabilities in Glioma.Cancers · 2026Review
- Patient-derived glioblastoma cultures preserve respiration phenotypes during ex vivo maintenance and show sex-associated differences in migration.Acta neuropathologica communications · 2026Article
- Label-Free Raman Spectroscopy Reveals Metabolic Signatures Associated with MGMT Promoter Methylation Status in Glioblastoma.Analytical chemistry · 2026Article
- Beyond Glycolysis: Targeting Non-Glycolytic Metabolic Pathways in Brain Tumors for Therapeutic Innovation: A Narrative Review.Health science reports · 2026Article
- Pharmacological Ascorbate Restrains Epithelial-Mesenchymal Transition and Invasion in Glioblastoma Cells via Extracellular HInternational journal of molecular sciences · 2026Article
- Article
- Review
- FLIM quality metric visualization as a means to validate consistency across large-area non-homogeneous FLIM datasets.Methods and applications in fluorescence · 2026Article
- Overcoming Chemoresistance in Glioblastoma: Mechanisms, Therapeutic Strategies, and Functional Precision Medicine.International journal of molecular sciences · 2026Review
- Metformin Suppresses Glioblastoma Tumor Growth and Progression Through the AMPK/FoxO3a/Survivin Axis.Cells · 2026Article
- Neutrophil Percentage-to-Albumin Ratio as a Novel Prognostic Biomarker in Adult Diffuse Gliomas: Retrospective Study Integrating 3 Machine Learning Models and Cox Regression.JMIR medical informatics · 2026Article
- C3G Downregulation Enhances Stemness in Glioblastoma Cells by Promoting PKM2 Upregulation.International journal of biological sciences · 2026Article
- Disrupting the TGF-β-regulated epithelial-mesenchymal transition, apoptotic and autophagic phenotypes of 3D glioblastoma spheroids via glycolytic inhibition.Exploration of targeted anti-tumor therapy · 2026Article
- Mechanistic role of glycolytic pathways in the tumor microenvironment in driving chemoresistance.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is one of the deadliest tumors due to its high aggressiveness and resistance to standard therapies, resulting in a dismal prognosis. This lethal tumor carries out metabolic reprogramming in order to modulate specific pathways, providing metabolites that promote GBM cells proliferation and limit the efficacy of standard treatments. Indeed, GBM remodels glucose metabolism and undergoes Warburg effect, fuelling glycolysis even when oxygen is available. Moreover, recent evidence revealed a rewiring in nucleotide, lipid and iron metabolism, resulting not only in an increased tumor growth, but also in radio- and chemo-resistance. Thus, while on the one hand metabolic reprogramming is an advantage for GBM, on the other hand it may represent an exploitable target to hamper GBM progression. Lately, a number of studies focused on drugs targeting metabolism to uncover their effects on tumor proliferation and therapy resistance, demonstrating that some of these are effective, in combination with conventional treatments, sensitizing GBM to radiotherapy and chemotherapy. However, GBM heterogeneity could lead to a plethora of metabolic alterations among subtypes, hence a metabolic treatment might be effective for proneural tumors but not for mesenchymal ones, which are more aggressive and resistant to conventional approaches. This review explores key mechanisms of GBM metabolic reprogramming and their involvement in therapy resistance, highlighting how metabolism acts as a double-edged sword for GBM, taking into account metabolic pathways that seem to offer promising treatment options for GBM.
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