ArticleCancers2022
Atovaquone: An Inhibitor of Oxidative Phosphorylation as Studied in Gynecologic Cancers.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 48 citations in OpenAlex.
- Re-evaluating the rationale for targeting oxidative phosphorylation in acute myeloid leukemia.The Biochemical journal · 2026Review
- Atovaquone Targets Mitochondrial Metabolism and Enhances Radiosensitivity of Diffuse Intrinsic Pontine Glioma.Cancers · 2026Article
- The oxidative phosphorylation inhibitor, atovaquone, upregulates PD-L1 via activation of the ATM/ATR DNA damage response pathway.Research square · 2026Article
- Mitochondria and tumorigenesis: Molecular basis and therapeutic implications.Genes & diseases · 2026Review
- Early Detection and Prevention of Ovarian Cancer.Cancers · 2025Review
- Targeted Therapies in Oral and Oropharyngeal Cancer: An Overview of Emerging and Repurposed Agents.Cancers · 2025Review
- Atovaquone-induced oxidative stress activates the pentose phosphate pathway and Immunogenic cell death in ovarian cancer.Scientific reports · 2025Article
- STAT3 axis in cancer and cancer stem cells: From oncogenesis to targeted therapies.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- MSN/STAT3 drives cancer stemness and chemoresistance via IL-6/LPAR1 ligand receptor complex in triple-negative breast cancer.Breast cancer research : BCR · 2025Article
- Article
- Atovaquone-induced activation of the PERK/eIF2α signaling axis mitigates metabolic radiosensitisation.Cell communication and signaling : CCS · 2025Article
- Data mining of PubChem bioassay records reveals diverse OXPHOS inhibitory chemotypes as potential therapeutic agents against ovarian cancer.Journal of cheminformatics · 2024Article
- Advances in ovarian tumor stem cells and therapy.Cell biochemistry and biophysics · 2024Review
- A Platelet-Powered Drug Delivery System for Enhancing Chemotherapy Efficacy for Liver Cancer Using the Trojan Horse Strategy.Pharmaceutics · 2024Article
- DPEP Inhibits Cancer Cell Glucose Uptake, Glycolysis and Survival by Upregulating Tumor Suppressor TXNIP.Cells · 2024Article
- Targeting the core program of metastasis with a novel drug combination.Cancer medicine · 2024Article
- Apigeninidin chloride disruptsFrontiers in cellular and infection microbiology · 2024Article
- Metabolic vulnerability of cancer stem cells and their niche.Frontiers in pharmacology · 2024Review
- Targeting Glucose Metabolism in Cancer Cells as an Approach to Overcoming Drug Resistance.Pharmaceutics · 2023Review
- Multifaceted roles of mitochondrial dysfunction in diseases: from powerhouses to saboteurs.Archives of pharmacal research · 2023Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Oxidative phosphorylation is an active metabolic pathway in cancer. Atovaquone is an oral medication that inhibits oxidative phosphorylation and is FDA-approved for the treatment of malaria. We investigated its potential anti-cancer properties by measuring cell proliferation in 2D culture. The clinical formulation of atovaquone, Mepron, was given to mice with ovarian cancers to monitor its effects on tumor and ascites. Patient-derived cancer stem-like cells and spheroids implanted in NSG mice were treated with atovaquone. Atovaquone inhibited the proliferation of cancer cells and ovarian cancer growth in vitro and in vivo. The effect of atovaquone on oxygen radicals was determined using flow and imaging cytometry. The oxygen consumption rate (OCR) in adherent cells was measured using a Seahorse XFe96 Extracellular Flux Analyzer. Oxygen consumption and ATP production were inhibited by atovaquone. Imaging cytometry indicated that the majority of the oxygen radical flux triggered by atovaquone occurred in the mitochondria. Atovaquone decreased the viability of patient-derived cancer stem-like cells and spheroids implanted in NSG mice. NMR metabolomics showed shifts in glycolysis, citric acid cycle, electron transport chain, phosphotransfer, and metabolism following atovaquone treatment. Our studies provide the mechanistic understanding and preclinical data to support the further investigation of atovaquone's potential as a gynecologic cancer therapeutic.
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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.