ArticleOncoscience2014
Disulfiram/copper causes redox-related proteotoxicity and concomitant heat shock response in ovarian cancer cells that is augmented by auranofin-mediated thioredoxin inhibition.
Article in Oncoscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Diethyldithiocarbamate-copper complex ignites the tumor microenvironment through NKG2D-NKG2DL axis.Frontiers in immunology · 2025Article
- Targeting cuproptosis for cancer therapy: mechanistic insights and clinical perspectives.Journal of hematology & oncology · 2024Review
- FDA-approved disulfiram as a novel treatment for aggressive leukemia.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Combination of the cuproptosis inducer disulfiram and anti‑PD‑L1 abolishes NSCLC resistance by ATP7B to regulate the HIF‑1 signaling pathway.International journal of molecular medicine · 2024Article
- Revolutionizing ovarian cancer therapy by drug repositioning for accelerated and cost-effective treatments.Frontiers in oncology · 2024Review
- Drug repositioning and ovarian cancer, a study based on Mendelian randomisation analysis.Frontiers in oncology · 2024Article
- Repurposed Drugs in Gastric Cancer.Molecules (Basel, Switzerland) · 2022Review
- Mouse pharmacokinetics and metabolism of the phenylurea thiocarbamate NSC 161128.Cancer chemotherapy and pharmacology · 2022Article
- Article
- Disulfiram in glioma: Literature review of drug repurposing.Frontiers in pharmacology · 2022Review
- Current Treatments and New Possible Complementary Therapies for Epithelial Ovarian Cancer.Biomedicines · 2021Review
- Alcohol-abuse drug disulfiram targets pediatric glioma via MLL degradation.Cell death & disease · 2021Article
- Evaluating Targeted Therapies in Ovarian Cancer Metabolism: Novel Role for PCSK9 and Second Generation mTOR Inhibitors.Cancers · 2021Article
- Therapeutic potential of endogenous hydrogen sulfide inhibition in breast cancer (Review).Oncology reports · 2021Review
- Review
- Targeting Aldehyde Dehydrogenases to Eliminate Cancer Stem Cells in Gynecologic Malignancies.Cancers · 2020Review
- Disulfiram causes selective hypoxic cancer cell toxicity and radio-chemo-sensitization via redox cycling of copper.Free radical biology & medicine · 2020Article
- Article
- Recent Advances in Antabuse (Disulfiram): The Importance of its Metal-binding Ability to its Anticancer Activity.Current medicinal chemistry · 2018Review
- BRCA1 and BRCA2 tumor suppressors protect against endogenous acetaldehyde toxicity.EMBO molecular medicine · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A valuable strategy to develop new therapeutic options for a variety of diseases has been the identification of new targets and applications for already approved drugs, the so-called drug repositioning. Recurrent ovarian cancer is a nearly incurable malignancy for which new and effective treatments are urgently needed. The alcohol-deterring drug disulfiram has been shown to cause preferential cell death in a variety of cancer cells. In this study, it is shown that disulfiram mediates effective cell death in ovarian cancer cells by promoting a pro-oxidative intracellular environment in a copper-dependent mechanism. Within few hours of application, disulfiram caused irreversible cell damage associated with pronounced induction of the inducible heat shock proteins HSP70, HSP40, and HSP32. The small heat shock protein HSP27 was found to be covalently dimerized via oxidized disulfide bonds and precipitated in para-nuclear protein aggregates. Simultaneous inhibition of the cellular thioredoxin system by auranofin further enhanced the cytotoxic effect of disulfiram. These data indeed indicate that the combination of two approved drugs, the anti-alcoholic disulfiram and the anti-rheumatic auranofin, may be of interest for the treatment of recurrent and genotoxic drug-resistant ovarian cancer by inducing a proteotoxic cell death mechanism.
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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.