ArticleJournal of ovarian research2024
Targeting mitochondrial metabolism with CPI-613 in chemoresistant ovarian tumors.
Article in Journal of ovarian research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Combination of lonidamine with devimistat induces synergistic antitumor effects in lung cancer via multifaceted disruption of cellular energy metabolism.Oncology reports · 2026Article
- Hyperpolarized [2-NMR in biomedicine · 2026Article
- Cell-Type-Resolved Proteomics Reveals Distinct Immune and Metabolic Programs Between Primary and Recurrent Ascites in HGSOC.Proteomics. Clinical applications · 2026Article
- MechAInistic: A Reviewer-Supervised Multi-Agent LLM System for Auditable Mechanistic Drug-Hypothesis Generation.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus.Molecular therapy. Oncology · 2026Article
- Aging-Driven Immunosuppression: The Role of Tregs in the Ovarian Tumor Microenvironment.Aging cell · 2026Article
- Spatiotemporal control of mitoribosome-mediated metabolic reprogramming in cancer: implications for heterogeneity and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- The Molecular Mechanism of a Complex1-induced Apoptosis in Cancer Cells of the Esophagus.Current molecular medicine · 2026Article
- GPT2 mediates glutamine metabolism-driven metabolic alterations in platinum-resistant ovarian cancer cells.Scientific reports · 2025Article
- Unlocking the mitochondrial functional code: unraveling the pathogenesis of ovarian cancer and innovative targets to inhibit malignant behavior.Journal of translational medicine · 2025Review
- Spatiotemporal Heterogeneity of Tumor Glucose Metabolism Reprogramming: From Single-Cell Mechanisms to Precision Interventions.International journal of molecular sciences · 2025Review
- Article
- Advances in α-Lipoic Acid for Disease Prevention: Mechanisms and Therapeutic Insights.Molecules (Basel, Switzerland) · 2025Review
- Metabolic Reprogramming Shapes the Progression and Therapeutic Landscape of Ovarian Cancer.Cancer management and research · 2025Review
- Article
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Authors and funding
14 authors.
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Abstract
backgroundThere is evidence indicating that chemoresistance in tumor cells is mediated by the reconfiguration of the tricarboxylic acid cycle, leading to heightened mitochondrial activity and oxidative phosphorylation (OXPHOS). Previously, we have shown that ovarian cancer cells that are resistant to chemotherapy display increased OXPHOS, mitochondrial function, and metabolic flexibility. To exploit this weakness in chemoresistant ovarian cancer cells, we examined the effectiveness of the mitochondrial inhibitor CPI-613 in treating preclinical ovarian cancer.
methodsChemosensitive OVCAR3, and chemoresistant CAOV3 and F2 ovarian cancer cells lines and their xenografts in nude mice were used. Functional metabolic studies were performed using Seahorse instrument. Metabolite quantification was performed using LC/MS/MS.
resultsMice treated with CPI-613 exhibited a notable increase in overall survival and a reduction in tumor development and burden in OVCAR3, F2, and CAOV3 xenografts. CPI-613 suppressed the activity of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase complex, which are two of its targets. This led to a reduction in OXPHOS and tricarboxylic acid cycle activity in all 3 xenografts. The addition of CPI-613 enhanced the responsiveness of chemotherapy in the chemoresistant F2 and CAOV3 tumors, resulting in a notable improvement in survival rates and a reduction in tumor size as compared to using chemotherapy alone. CPI-613 reduced the chemotherapy-induced OXPHOS in chemoresistant tumors. The study revealed that the mechanism by which CPI-613 inhibits tumor growth is through mitochondrial collapse. This is evidenced by an increase in superoxide production within the mitochondria, a decrease in ATP generation, and the release of cytochrome C, which triggers mitochondria-induced apoptosis.
conclusionOur study demonstrates the translational potential of CPI-613 against chemoresistant ovarian tumors.
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