ArticleCancer cell international2022
Etomoxir, a carnitine palmitoyltransferase 1 inhibitor, combined with temozolomide reduces stemness and invasiveness in patient-derived glioblastoma tumorspheres.
Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 62 citations in OpenAlex.
- Metabolite ratiomics: Rapid diagnosis and classification of gliomas for intraoperative application during brain surgery.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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- The Unsaturated/Saturated Fatty Acid Ratio: A Metabolic Hub and Therapeutic Vulnerability in Glioblastoma.Biomedicines · 2026Review
- Beyond Glycolysis: Targeting Non-Glycolytic Metabolic Pathways in Brain Tumors for Therapeutic Innovation: A Narrative Review.Health science reports · 2026Article
- The metabolic profiles of cancer stem cells.Stem cell research & therapy · 2026Review
- Metabolic crosstalk among cancer-associated fibroblasts, adipocytes and immune cells as an immunosuppressive tumor microenvironment driver.Experimental & molecular medicine · 2026Review
- Acylcarnitines in Cancer Metabolism: Mechanistic Insights and Stratification Potential.Cancers · 2026Review
- Targeting metabolic mechanisms to overcome temozolomide resistance in glioblastoma.Discover oncology · 2026Review
- Pharmacological transglutaminase 2 inhibition enhances temozolomide response in patient-derived glioblastoma tumorspheres.Journal of neuro-oncology · 2026Article
- Implantation of engineered adipocytes suppresses tumor progression in cancer models.Nature biotechnology · 2025Article
- HIF-1 attenuates high-fiber diet-mediated proliferation and stemness of colonic epithelium.Gut microbes · 2025Article
- Novel therapeutic strategies for targeting fatty acid oxidation in cancer.Biomarker research · 2025Review
- Myeloid metabolism and its role in immunotherapy of cancer.Journal for immunotherapy of cancer · 2025Review
- Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.Journal of translational medicine · 2025Review
- Targeting the Mitochondria in High-Grade Gliomas.Cancers · 2025Review
- Review
- Focused ultrasound-mediated temozolomide delivery into intact blood-brain barrier tissue improves survival in patient-derived xenograft model of glioblastoma.Fluids and barriers of the CNS · 2025Article
- Metabolic Adaptations in Cancer Progression: Optimization Strategies and Therapeutic Targets.Cancers · 2025Review
- Emerging roles for fatty acid oxidation in cancer.Genes & diseases · 2025Review
- Case report of three patients with end-stage recurrent glioblastoma treated with meldonium.BJC reports · 2025Article
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Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
Abstract
introductionThe importance of fatty acid oxidation (FAO) in the bioenergetics of glioblastoma (GBM) is being realized. Etomoxir (ETO), a carnitine palmitoyltransferase 1 (CPT1) inhibitor exerts cytotoxic effects in GBM, which involve interrupting the FAO pathway. We hypothesized that FAO inhibition could affect the outcomes of current standard temozolomide (TMZ) chemotherapy against GBM.
methodsThe FAO-related gene expression was compared between GBM and the tumor-free cortex. Using four different GBM tumorspheres (TSs), the effects of ETO and/or TMZ was analyzed on cell viability, tricarboxylate (TCA) cycle intermediates and adenosine triphosphate (ATP) production to assess metabolic changes. Alterations in tumor stemness, invasiveness, and associated transcriptional changes were also measured. Mouse orthotopic xenograft model was used to elucidate the combinatory effect of TMZ and ETO.
resultsGBM tissues exhibited overexpression of FAO-related genes, especially CPT1A, compared to the tumor-free cortex. The combined use of ETO and TMZ further inhibited TCA cycle and ATP production than single uses. This combination treatment showed superior suppression effects compared to treatment with individual agents on the viability, stemness, and invasiveness of GBM TSs, as well as better downregulation of FAO-related gene expression. The results of in vivo study showed prolonged survival outcomes in the combination treatment group.
conclusionETO, an FAO inhibitor, causes a lethal energy reduction in the GBM TSs. When used in combination with TMZ, ETO effectively reduces GBM cell stemness and invasiveness and further improves survival. These results suggest a potential novel treatment option for GBM.
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