ArticleScientific reports2019
Lipid accumulation and oxidation in glioblastoma multiforme.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 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.
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Who cites it
88 citing papers in PubMed, 146 citations in OpenAlex.
- Matrix stress relaxation drives glioblastoma cell response in viscoelastic biomaterials.Science advances · 2026Article
- The Unsaturated/Saturated Fatty Acid Ratio: A Metabolic Hub and Therapeutic Vulnerability in Glioblastoma.Biomedicines · 2026Review
- The Hallmarks of Glioblastoma: Functional Interplay Between Long Non-Coding RNAs and RNA-Binding Proteins.Cells · 2026Review
- BRI3 Orchestrates Lipid Metabolism and Autophagy in Glioblastoma: Implications for Tumor Cell Resilience.Biochemical genetics · 2026Article
- ARNT2 repression disrupts neuronal identity and promotes glioblastoma growth.Cell communication and signaling : CCS · 2026Article
- Targeting Metabolic Vulnerabilities in Glioblastoma: a Framework for Multi-node Combination Therapy.Current oncology reports · 2026Review
- Enhanced lipid metabolism serves as a metabolic vulnerability to polyunsaturated fatty acids in glioblastoma.JCI insight · 2026Article
- Lipid metabolic plasticity in glioblastoma: mechanisms, tumor microenvironment remodeling, and therapeutic opportunities.Frontiers in oncology · 2026Review
- Metabolic reprogramming and immunosenescence: a new sight for glioma therapy.Frontiers in cell and developmental biology · 2026Review
- Loss of CDS1 impairs the tumorigenic characteristics of nasopharyngeal carcinoma by modulating lipid metabolism.Cell adhesion & migration · 2025Article
- Exploring the diagnostic and prognostic potential of LCFAs' metabolic and biosynthetic pathways in glioblastoma multiforme using a bioinformatics approach.Research in pharmaceutical sciences · 2025Article
- Article
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Glioblastoma: From Pathophysiology to Novel Therapeutic Approaches.Biomedicines · 2025Review
- Triglyceride metabolism controls inflammation and microglial phenotypes associated with APOE4.Cell reports · 2025Article
- The Warburg hypothesis and the emergence of the mitochondrial metabolic theory of cancer.Journal of bioenergetics and biomembranes · 2025Review
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- TRAF3 loss protects glioblastoma cells from lipid peroxidation and immune elimination via dysregulated lipid metabolism.The Journal of clinical investigation · 2025Article
- The RET inhibitor pralsetinib suppresses TMZ-resistant glioma growth by regulating spermine production.Frontiers in pharmacology · 2025Article
- CD36 as a Therapeutic Target in Tumor Microenvironment and Lipid Metabolism.Anti-cancer agents in medicinal chemistry · 2025Review
28 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
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most common and lethal primary malignant brain tumor in adults. Despite the multimodal standard treatments for GBM, the median survival is still about one year. Analysis of brain tissues from GBM patients shows that lipid droplets are highly enriched in tumor tissues while undetectable in normal brain tissues, yet the identity and functions of lipid species in GBM are not well understood. The aims of the present work are to determine how GBM utilizes fatty acids, and assess their roles in GBM proliferation. Treatment of U138 GBM cells with a monounsaturated fatty acid, oleic acid, induces accumulation of perilipin 2-coated lipid droplets containing triglycerides enriched in C18:1 fatty acid, and increases fatty acid oxidation. Interestingly, oleic acid also increases glucose utilization and proliferation of GBM cells. In contrast, pharmacologic inhibition of monoacylglycerol lipase attenuates GBM proliferation. Our findings demonstrate that monounsaturated fatty acids promote GBM proliferation via triglyceride metabolism, suggesting a novel lipid droplet-mediated pathway which may be targeted for GBM treatment.
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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.