ArticleRedox biology2020
Phenotypic screen for oxygen consumption rate identifies an anti-cancer naphthoquinone that induces mitochondrial oxidative stress.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed.
- Modeling the metabolic response of A2780 ovarian cancer cells to gold-based cytotoxic drugs.NPJ systems biology and applications · 2025Article
- Empagliflozin Inhibits Neuronal Ferroptosis Induced by Oxygen-Glucose Deprivation/Reoxygenation by Activating the Nrf2/HO-1 Pathway.Molecular neurobiology · 2025Article
- Design, Synthesis, and Biological Evaluation of Naphthoquinone Salts as Anticancer Agents.Molecules (Basel, Switzerland) · 2025Article
- Molecular Docking and Dynamics Simulation Studies Predict Potential Anti-ADAR2 Inhibitors: Implications for the Treatment of Cancer, Neurological, Immunological and Infectious Diseases.International journal of molecular sciences · 2023Article
- Chemopreventive Effects ofCurrent issues in molecular biology · 2023Article
- Ceria nanoparticles ameliorate renal fibrosis by modulating the balance between oxidative phosphorylation and aerobic glycolysis.Journal of nanobiotechnology · 2022Article
- Increased glucosylceramide production leads to decreased cell energy metabolism and lowered tumor marker expression in non-cancerous liver cells.Cellular and molecular life sciences : CMLS · 2021Article
- Kaempferol Ameliorates Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Ferroptosis by Activating Nrf2/SLC7A11/GPX4 Axis.Biomolecules · 2021Article
- Role of mitochondrial quality control in the pathogenesis of nonalcoholic fatty liver disease.Aging · 2020Review
Corrections and comments
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Authors and funding
25 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hallmark of cancer cells is their ability to reprogram nutrient metabolism. Thus, disruption to this phenotype is a potential avenue for anti-cancer therapy. Herein we used a phenotypic chemical library screening approach to identify molecules that disrupted nutrient metabolism (by increasing cellular oxygen consumption rate) and were toxic to cancer cells. From this screen we discovered a 1,4-Naphthoquinone (referred to as BH10) that is toxic to a broad range of cancer cell types. BH10 has improved cancer-selective toxicity compared to doxorubicin, 17-AAG, vitamin K3, and other known anti-cancer quinones. BH10 increases glucose oxidation via both mitochondrial and pentose phosphate pathways, decreases glycolysis, lowers GSH:GSSG and NAPDH/NAPD
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Registered trials
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