ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2024
A gold-based inhibitor of oxidative phosphorylation is effective against triple negative breast cancer.
Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- TMEM70 drives breast cancer progression via mitochondrial oxidative phosphorylation and microenvironment remodeling.Cancer cell international · 2026Article
- Triple-negative breast cancer: challenges, advances, and promising therapeutic interventions.Medical oncology (Northwood, London, England) · 2025Review
- Advances in nanoparticle-based doxorubicin delivery: precision strategies for targeted treatment of triple-negative breast cancer.Discover nano · 2025Review
- Leveraging Immunogenic Cell Death to Enhance the Immune Response against Malignant Pleural Mesothelioma Tumors.Journal of the American Chemical Society · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is associated with metabolic heterogeneity and poor prognosis with limited treatment options. New treatment paradigms for TNBC remains an unmet need. Thus, therapeutics that target metabolism are particularly attractive approaches. We previously designed organometallic Au(III) compounds capable of modulating mitochondrial respiration by ligand tuning with high anticancer potency in vitro and in vivo. Here, we show that an efficacious Au(III) dithiocarbamate (AuDTC) compound induce mitochondrial dysfunction and oxidative damage in cancer cells. Efficacy of AuDTC in TNBC mouse models harboring mitochondrial oxidative phosphorylation (OXPHOS) dependence and metabolic heterogeneity establishes its therapeutic potential following systemic delivery. This provides evidence that AuDTC is an effective modulator of mitochondrial respiration worthy of clinical development in the context of TNBC. ONE SENTENCE SUMMARY: Metabolic-targeting of triple-negative breast cancer by gold anticancer agent may provide efficacious therapy.
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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.