ArticlePLoS biology2018
Identifying off-target effects of etomoxir reveals that carnitine palmitoyltransferase I is essential for cancer cell proliferation independent of β-oxidation.
Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 1 of them a synthesis that pooled it.
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Who cites it
141 citing papers in PubMed, 1 synthesis or guideline pooled it, 192 citations in OpenAlex.
- Metabolic regulation and immunosuppressive functions of lipid-associated macrophages in pancreatic ductal adenocarcinoma.Frontiers in immunology · 2026Pooled it
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- miR-146a mimic therapy protects against platelet-mediated thrombosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Lipid metabolic reprogramming of tumor-associated macrophages drives resistance to immune checkpoint blockade in lung cancer: a narrative review of mechanisms and therapeutic strategies.Translational lung cancer research · 2026Review
- Fatty acid oxidation fuels mitochondrial respiration to drive epidermal stem cell fate and differentiation.Nature communications · 2026Article
- The Unsaturated/Saturated Fatty Acid Ratio: A Metabolic Hub and Therapeutic Vulnerability in Glioblastoma.Biomedicines · 2026Review
- Energy substrate preference and metabolic flexibility in quiescent and oxytocin-stimulated human myometrial cells.iScience · 2026Article
- PSMC2 drives tumor progression in nasopharyngeal carcinoma by inhibiting ferroptosis through STAT3.Discover oncology · 2026Article
- Enhanced fatty acid availability rewires fibroblasts metabolism and decreases collagen deposition in lung fibrosis.Cellular and molecular life sciences : CMLS · 2026Article
- Plasma acylcarnitine dysregulation associated with CPT1-mediated metabolism contributes to oral carcinogenesis.Scientific reports · 2026Article
- Energetic diversity in retinal ganglion cells is modulated by neuronal activity and correlates with resilience to degeneration.Nature communications · 2026Article
- Drug Repurposing in Oncology: A Strategic Pathway to Unlocking New Therapeutic Potential.Therapeutic innovation & regulatory science · 2026Review
- Mechanism-based new approach methodologies for in vitro detection of chemical-induced liver steatosis.Archives of toxicology · 2026Review
- Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.Frontiers in cell and developmental biology · 2026Review
- The emerging metabolic role and treatment target of CPT1A in CRC.Frontiers in cell and developmental biology · 2026Review
- ACSL5 programs fatty acid metabolism and mitochondrial fitness to sustain pathogenic T cells and exacerbate Sjögren's syndrome.International journal of biological sciences · 2026Article
- Metabolic licensing and restriction of innate immunity in the tumor microenvironment.Frontiers in immunology · 2026Review
- Transient exposure to bisphenol F in early life affects the metabolic health of adults.Exposome · 2026Article
- CPT1A as a metabolic gatekeeper linking fatty acid oxidation, ferroptosis resistance, and breast cancer stemness.Frontiers in oncology · 2026Review
- Catabolic rewiring in cancer impacts dietary interventions.Communications biology · 2025Review
81 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
It has been suggested that some cancer cells rely upon fatty acid oxidation (FAO) for energy. Here we show that when FAO was reduced approximately 90% by pharmacological inhibition of carnitine palmitoyltransferase I (CPT1) with low concentrations of etomoxir, the proliferation rate of various cancer cells was unaffected. Efforts to pharmacologically inhibit FAO more than 90% revealed that high concentrations of etomoxir (200 μM) have an off-target effect of inhibiting complex I of the electron transport chain. Surprisingly, however, when FAO was reduced further by genetic knockdown of CPT1, the proliferation rate of these same cells decreased nearly 2-fold and could not be restored by acetate or octanoic acid supplementation. Moreover, CPT1 knockdowns had altered mitochondrial morphology and impaired mitochondrial coupling, whereas cells in which CPT1 had been approximately 90% inhibited by etomoxir did not. Lipidomic profiling of mitochondria isolated from CPT1 knockdowns showed depleted concentrations of complex structural and signaling lipids. Additionally, expression of a catalytically dead CPT1 in CPT1 knockdowns did not restore mitochondrial coupling. Taken together, these results suggest that transport of at least some long-chain fatty acids into the mitochondria by CPT1 may be required for anabolic processes that support healthy mitochondrial function and cancer cell proliferation independent of FAO.
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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.