ArticleJournal of gastrointestinal oncology2020
Enhanced fatty acid oxidation mediated by CPT1C promotes gastric cancer progression.
Article in Journal of gastrointestinal oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- Multifunctional Role of Mitochondrial Fatty Acid Oxidation in Cancer Immunotherapy and Aging.Cancer science · 2026Review
- Combining machine learning and multi-omics analysis to explore the role of CPT1C in colorectal tumor cancer transformation.Scientific reports · 2026Article
- Exploring the significance of fatty acid metabolism reprogramming in the pathogenesis of cancer and anticancer therapy.Annals of medicine · 2025Review
- A Bioinformatics-Driven ceRNA Network in Stomach Adenocarcinoma: Identification of Novel Prognostic mRNA-miRNA-lncRNA Interactions.Medical sciences (Basel, Switzerland) · 2025Article
- Mesenchymal stem cell-derived lncRNAs NKILA contributes to stemness and chemoresistance by fatty acid oxidation in gastric cancerWorld journal of gastrointestinal oncology · 2025Article
- Carnitine palmitoyltransferase 1C promotes EMT-associated cisplatin resistance in non-small cell lung cancer cells.Cancer biology & medicine · 2025Article
- Review
- Metabolomic machine learning predictor for diagnosis and prognosis of gastric cancer.Nature communications · 2024Article
- The genomic alterations in glioblastoma influence the levels of CSF metabolites.Acta neuropathologica communications · 2024Article
- Article
- CPT1C-positive cancer-associated fibroblast facilitates immunosuppression through promoting IL-6-induced M2-like phenotype of macrophage.Oncoimmunology · 2024Article
- Identification of bladder cancer subtypes and predictive model for prognosis, immune features, and immunotherapy based on neutrophil extracellular trap-related genes.Scientific reports · 2023Article
- The Physiological and Pathological Role of Acyl-CoA Oxidation.International journal of molecular sciences · 2023Review
- CPT1C-mediated fatty acid oxidation facilitates colorectal cancer cell proliferation and metastasis.Acta biochimica et biophysica Sinica · 2023Article
- The Association of Circulating L-Carnitine, γ-Butyrobetaine and Trimethylamine N-Oxide Levels with Gastric Cancer.Diagnostics (Basel, Switzerland) · 2023Article
- To be or not to be a fat burner, that is the question for cpt1c in cancer cells.Cell death & disease · 2023Review
- Cpt1c Downregulation Causes Plasma Membrane Remodelling and Anthracycline Resistance in Breast Cancer.International journal of molecular sciences · 2023Article
- Metabolic Flux Analysis Reveals the Roles of Stearate and Oleate on CPT1C-mediated Tumor Cell Senescence.International journal of biological sciences · 2023Article
- Clinical Utility of Ivosidenib in the Treatment of IDH1-Mutant Cholangiocarcinoma: Evidence To Date.Cancer management and research · 2023Review
- The prognostic role of fatty acid metabolism-related genes in patients with gastric cancer.Translational cancer research · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCarnitine palmitoyltransferase 1C (CPT1C) is a critical enzyme that catalyzes carnitinylation of fatty acids for transport into mitochondria for β-oxidation. No previous studies have been conducted to explore the prognostic and oncogenic role of CPT1C in gastric cancer (GC).
methodsPublic RNA-sequencing data and micro-array data were extracted from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases respectively. Survival analysis was performed in TCGA and GSE62254 cohorts. RT-qPCR and Western blot analyses were used to determine genes expression in GC cells. Fatty acid oxidation (FAO) assay kit was used to examine cell FAO rate. The cell proliferation ability and cell cycle were tested by using CCK-8 and cell cycle assay kits.
resultsIn the both TCGA and GSE62254 cohorts, high expression of CPT1C was significantly associated with poor overall (OS) (P<0.001) and disease free survival (DFS) of GC patients (P<0.001). Silence of CPT1C significantly inhibited cell FAO rate, suppressed cell proliferation and induced cell cycle arrest, while enforced CPT1C expression had the opposite effects. However, etomoxir treatment completely restricted the increase of FAO rate, cell viability and the phase of DNA synthesis caused by enhanced CPT1C expression. Of note, CPT1C expression was transcriptionally activated by hypoxia inducible factor-1α.
conclusionsHigh expression of CPT1C induced by hypoxia was closely associated with poor prognosis and can promote proliferation of GC cells.
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