ArticleJournal of advanced research2026
Mitochondrial fatty acid oxidation as the target for blocking therapy-resistance and inhibiting tumor recurrence: The proof-of-principle model demonstrated for ovarian cancer cells.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Dissecting residual disease in spheroids reveals pan-cancer persistence signatures and a therapeutic window for oncolytic viruses.Molecular therapy. Oncology · 2026Article
- Metabolic Reprogramming of Cancer Stem Cells: Targeting Lipid Flux and Mitochondrial Plasticity to Overcome Therapeutic Resistance.Cancer medicine · 2026Review
- Drug-tolerant persister cells in cancer: a scoping review of definitions, models, and molecular mechanisms.Frontiers in oncology · 2026Review
- Advancing the frontiers of ovarian cancer therapy: a comprehensive synthesis of emerging cell death paradigms.Oncology reviews · 2026Review
- Precision oncology in gynecologic cancers: molecular taxonomy, biomarker-guided therapeutics, and the challenge of therapeutic resistance.Frontiers in oncology · 2026Review
- Role of the tumor microenvironment in chemotherapy resistance in ovarian cancer and targeted therapy.Journal of ovarian research · 2025Review
- Mitochondrial Metabolomics in Cancer: Mass Spectrometry-Based Approaches for Metabolic Rewiring Analysis and Therapeutic Discovery.Metabolites · 2025Review
- Metabolic Reprogramming Shapes the Progression and Therapeutic Landscape of Ovarian Cancer.Cancer management and research · 2025Review
- Targeting lipid metabolic vulnerabilities with small-molecule inhibitors in acute myeloid leukemia: Emerging insights and therapeutic opportunities.Tzu chi medical journalReview
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16 authors.
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Abstract
introductionCancer patients treated with current chemotherapeutic and targeted therapies frequently achieve partial remission, which ultimately relapse with more aggressive, drug-resistant tumor phenotypes. To a certain extent, drug-tolerant persister (DTP) cells are responsible for residual tumors after systemic anticancer therapy and the onset of acquired drug resistance. Therefore, novel therapies targeting DTP cells to prevent drug resistance and tumor recurrence are urgently needed.
objectivesWe aimed to investigate the traits and key vulnerabilities of drug-tolerant ovarian cancer persister cells and to seek out potential therapeutic strategies.
methodsWe constructed paclitaxel-tolerant ovarian cancer persister cells by exposing ovarian cancer parental cells to a lethal dose of paclitaxel. Proteomics analysis, in vitro and in vivo assays were performed to identify biological processes that could serve as potential vulnerabilities in persister cells.
resultsPaclitaxel-tolerant ovarian cancer persister cells were found to undergo a metabolic reprogramming through the upregulation of fatty acid oxidation (FAO). Treatment with the FAO inhibitor ST1326 suppressed FAO and increased sensitivity to paclitaxel in persister cells. Moreover, combination therapy with paclitaxel and ST1326 prevented ovarian tumor recurrence with satisfactory biosafety in a mouse model of ovarian cancer relapse, indicating that FAO disruption can improve the efficacy of paclitaxel-based therapy in ovarian cancer. Mechanistically, we found that paclitaxel treatment upregulated CEBPB, a transcription factor that induced the expression of the FAO-related enzyme HADHA and contributed to FAO elevation in persister cells.
conclusionsThis study revealed an upregulation of FAO in paclitaxel-tolerant ovarian cancer persister cells and provided a prospective paclitaxel-ST1326 combination therapy targeting persister cells that may prevent the development of acquired drug resistance and achieve superior long-term ovarian cancer control in the future. Our research established a conceptual framework for advancing personalized treatment approaches and enhancing patient outcomes in ovarian cancer therapy.
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