ArticleOncotarget2017
Auranofin radiosensitizes tumor cells through targeting thioredoxin reductase and resulting overproduction of reactive oxygen species.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 91 citations in OpenAlex.
- Tumor cell membrane‑coated MOF‑199 nanoparticles co‑loaded with auranofin and celecoxib enhance single‑dose radiotherapy and anti‑PD‑L1 therapy in cervical cancer.Journal of nanobiotechnology · 2026Article
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- Nanomaterials reshaping cancer radiotherapy: Radiosensitization mechanisms, delivery and theranostic platforms, multimodal synergy, and clinical translation strategies.Materials today. Bio · 2026Review
- Redox rewiring in glioblastoma: the thioredoxin system as a precision therapeutic target.Pharmacological reports : PR · 2026Review
- Reactive oxygen species promotion drives auranofin's antiviral activity against hepatitis E virus.Journal of virology · 2026Article
- Evaluating the Antiproliferative Effects of Tri(2-Furyl)- and Triphenylphosphine-Gold(I) Pyridyl- and Pyrimidine-Thiolate Complexes.Biomolecules · 2026Article
- Redox Modulation in Therapy of Cancer: Some Pros and Cons.Antioxidants (Basel, Switzerland) · 2025Review
- Anti-Tumoral Treatment with Thioredoxin Reductase 1 Inhibitor Auranofin Fosters Regulatory T Cell and B16F10 Expansion in Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Living on the Edge: ROS Homeostasis in Cancer Cells and Its Potential as a Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- Beyond gold: the chemoenhancing mechanism and therapeutic potential of auranofin in melanoma.Cancer biology & medicine · 2025Article
- CRISPR screen reveals a simultaneous targeted mechanism to reduce cancer cell selenium and increase lipid oxidation to induce ferroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mitoregulin Promotes Cell Cycle Progression in Non-Small Cell Lung Cancer Cells.International journal of molecular sciences · 2025Article
- Auranofin inhibition of thioredoxin reductase sensitizes lung neuroendocrine tumor cells (NETs) and small cell lung cancer (SCLC) cells to sorafenib as well as inhibiting SCLC xenograft growth.Cancer biology & therapy · 2024Article
- Auranofin as a Novel Anticancer Drug for Anaplastic Thyroid Cancer.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Thioredoxin System Protein Expression in Carcinomas of the Pancreas, Distal Bile Duct, and Ampulla in the United Kingdom.Diseases (Basel, Switzerland) · 2024Article
- Exploring the Thioredoxin System as a Therapeutic Target in Cancer: Mechanisms and Implications.Antioxidants (Basel, Switzerland) · 2024Review
- Feedback loop between hypoxia and energy metabolic reprogramming aggravates the radioresistance of cancer cells.Experimental hematology & oncology · 2024Review
- Article
- Ferroptosis: Frenemy of Radiotherapy.International journal of molecular sciences · 2024Review
- Auranofin Inhibition of Thioredoxin Reductase Sensitizes Lung Neuroendocrine Tumor Cells (NETs) and Small Cell Lung Cancer (SCLC) Cells to Sorafenib as well as Inhibiting SCLC Xenograft Growth.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Auranofin (AF) is an anti-arthritic drug considered for combined chemotherapy due to its ability to impair the redox homeostasis in tumor cells. In this study, we asked whether AF may in addition radiosensitize tumor cells by targeting thioredoxin reductase (TrxR), a critical enzyme in the antioxidant defense system operating through the reductive protein thioredoxin. Our principal findings in murine 4T1 and EMT6 tumor cells are that AF at 3-10 μM is a potent radiosensitizer in vitro, and that at least two mechanisms are involved in TrxR-mediated radiosensitization. The first one is linked to an oxidative stress, as scavenging of reactive oxygen species (ROS) by N-acetyl cysteine counteracted radiosensitization. We also observed a decrease in mitochondrial oxygen consumption with spared oxygen acting as a radiosensitizer under hypoxic conditions. Overall, radiosensitization was accompanied by ROS overproduction, mitochondrial dysfunction, DNA damage and apoptosis, a common mechanism underlying both cytotoxic and antitumor effects of AF. In tumor-bearing mice, a simultaneous disruption of the thioredoxin and glutathione systems by the combination of AF and buthionine sulfoximine was shown to significantly improve tumor radioresponse. In conclusion, our findings illuminate TrxR in cancer cells as an exploitable radiobiological target and warrant further validation of AF in combination with radiotherapy.
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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.