ArticleCancers2019
The Metabolic Inhibitor CPI-613 Negates Treatment Enrichment of Ovarian Cancer Stem Cells.
Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- A comprehensive overview of ovarian cancer stem cells: correlation with high recurrence rate, underlying mechanisms, and therapeutic opportunities.Molecular cancer · 2025Review
- The metabolic landscape of ovarian cancer stem cells: how do they survive?Frontiers in oncology · 2025Review
- From gut to proteomics: the impact ofFrontiers in oncology · 2025Article
- Metabolic Reprogramming Shapes the Progression and Therapeutic Landscape of Ovarian Cancer.Cancer management and research · 2025Review
- Targeting mitochondrial metabolism with CPI-613 in chemoresistant ovarian tumors.Journal of ovarian research · 2024Article
- Metabolic vulnerability of cancer stem cells and their niche.Frontiers in pharmacology · 2024Review
- Inhibition of TCA cycle improves the anti-PD-1 immunotherapy efficacy in melanoma cells via ATF3-mediated PD-L1 expression and glycolysis.Journal for immunotherapy of cancer · 2023Article
- Transcription factor Nkx2-3 maintains the self-renewal of hematopoietic stem cells by regulating mitophagy.Leukemia · 2023Article
- Succinate based polymers drive immunometabolism in dendritic cells to generate cancer immunotherapy.Journal of controlled release : official journal of the Controlled Release Society · 2023Article
- "DEPHENCE" system-a novel regimen of therapy that is urgently needed in the high-grade serous ovarian cancer-a focus on anti-cancer stem cell and anti-tumor microenvironment targeted therapies.Frontiers in oncology · 2023Review
- The evolving role of DNA damage response in overcoming therapeutic resistance in ovarian cancer.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Mitochondrial Matrix Protease ClpP Agonists Inhibit Cancer Stem Cell Function in Breast Cancer Cells by Disrupting Mitochondrial Homeostasis.Cancer research communications · 2022Article
- Blockade of glutamine-dependent cell survival augments antitumor efficacy of CPI-613 in head and neck cancer.Journal of experimental & clinical cancer research : CR · 2021Article
- Inhibition of Mitochondrial Metabolism Leads to Selective Eradication of Cells Adapted to Acidic Microenvironment.International journal of molecular sciences · 2021Article
- Identification of PDHX as a metabolic target for esophageal squamous cell carcinoma.Cancer science · 2021Article
- Article
- Review
- Is Mitochondrial Dysfunction a Common Root of Noncommunicable Chronic Diseases?Endocrine reviews · 2020Review
- Redox Homeostasis and Metabolism in Cancer: A Complex Mechanism and Potential Targeted Therapeutics.International journal of molecular sciences · 2020Review
- CPI-613 rewires lipid metabolism to enhance pancreatic cancer apoptosis via the AMPK-ACC signaling.Journal of experimental & clinical cancer research : CR · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
One of the most significant therapeutic challenges in the treatment of ovarian cancer is the development of recurrent platinum-resistant disease. Cancer stem cells (CSCs) are postulated to contribute to recurrent and platinum-resistant ovarian cancer (OvCa). Drugs that selectively target CSCs may augment the standard of care cytotoxics and have the potential to prevent and/or delay recurrence. Increased reliance on metabolic pathway modulation in CSCs relative to non-CSCs offers a possible therapeutic opportunity. We demonstrate that treatment with the metabolic inhibitor CPI-613 (devimistat, an inhibitor of tricarboxylic acid (TCA) cycle) in vitro decreases CD133+ and CD117+ cell frequency relative to untreated OvCa cells, with negligible impact on non-CSC cell viability. Additionally, sphere-forming capacity and tumorigenicity in vivo are reduced in the CPI-613 treated cells. Collectively, these results suggest that treatment with CPI-613 negatively impacts the ovarian CSC population. Furthermore, CPI-613 impeded the unintended enrichment of CSC following olaparib or carboplatin/paclitaxel treatment. Collectively, our results suggest that CPI-613 preferentially targets ovarian CSCs and could be a candidate to augment current treatment strategies to extend either progression-free or overall survival of OvCa.
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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.