ArticleRedox biology2021
Auranofin reveals therapeutic anticancer potential by triggering distinct molecular cell death mechanisms and innate immunity in mutant p53 non-small cell lung cancer.
Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Metallodrugs in the battle against non-small cell lung cancer: unlocking the potential for improved therapeutic outcomes.Frontiers in pharmacology · 2023Pooled it
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- Selenoproteins: Minute yet vital players governing cellular fate.Genes & diseases · 2026Review
- Co-treatment of Colchicine and Rosiglitazone synergistically inhibits cytokine-driven inflammation and modulates the related hsa-miRNA26a-5p, hsa-miRNA21-5p, and STAT3 expression in non-small cell lung cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Apoptosis execution is spatially regulated.Apoptosis : an international journal on programmed cell death · 2026Article
- Metal-dependent regulated cell death: Molecular architecture and translational frontiers.iMeta · 2026Review
- Ferroptosis vulnerability of enzalutamide resistant prostate cancer conferred by ACSL4 overexpression and GPX4 antagonism.Cell death & disease · 2026Article
- Context‑dependent targeting of thioredoxin reductase 1 in cancer: a mechanistic review.Magyar onkologia · 2026Review
- Programmed cell death in lung cancer: mechanisms, immune responses, and therapeutics.Apoptosis : an international journal on programmed cell death · 2026Review
- Viral mimicry may help explain immunogenic cell death.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Auranofin Combination Therapy: A New Frontier in Cancer Treatment.Molecules (Basel, Switzerland) · 2026Review
- Organoplatinum(II) Type II Immunogenic Cell Death Inducers Target Protein Tyrosine Phosphatase 1B to Drive Immunogenicity.Journal of the American Chemical Society · 2026Article
- Targeting regulated cell death pathways in lung cancer: mechanisms, therapeutic strategies, and clinical translation.Frontiers in immunology · 2026Review
- KNL1 Regulates Ferroptosis Resistance and Migration in Lung Adenocarcinoma Cells via AMPK-mTOR Signaling.Oncology research · 2026Article
- HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025Review
- Combination nitazoxanide and auranofin treatment has synergistic anticancer activity in anaplastic thyroid cancer through enhanced activation of oxidative stress that leads to apoptosis.Cancer letters · 2025Article
- Synthesis and in vitro characterization of [EJNMMI radiopharmacy and chemistry · 2025Article
- Rewiring cancer metabolism: oncogenic signaling pathways and targeted therapeutics.Science China. Life sciences · 2025Review
- Targeted ferroptosis induction enhances chemotherapy efficacy in chemoresistant neuroblastoma.NPJ precision oncology · 2025Article
- A predictive serum miRNA signature impacts diffuse large B-cell lymphoma cell viability via inhibition of EGLN1 and TXNRD1 regulators of ferroptosis.British journal of haematology · 2025Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Auranofin (AF) is an FDA-approved antirheumatic drug with anticancer properties that acts as a thioredoxin reductase 1 (TrxR) inhibitor. The exact mechanisms through which AF targets cancer cells remain elusive. To shed light on the mode of action, this study provides an in-depth analysis on the molecular mechanisms and immunogenicity of AF-mediated cytotoxicity in the non-small cell lung cancer (NSCLC) cell line NCI-H1299 (p53 Null) and its two isogenic derivates with mutant p53 R175H or R273H accumulation. TrxR is highly expressed in a panel of 72 NSCLC patients, making it a valid druggable target in NSCLC for AF. The presence of mutant p53 overexpression was identified as an important sensitizer for AF in (isogenic) NSCLC cells as it was correlated with reduced thioredoxin (Trx) levels in vitro. Transcriptome analysis revealed dysregulation of genes involved in oxidative stress response, DNA damage, granzyme A (GZMA) signaling and ferroptosis. Although functionally AF appeared a potent inhibitor of GPX4 in all NCI-H1299 cell lines, the induction of lipid peroxidation and consequently ferroptosis was limited to the p53 R273H expressing cells. In the p53 R175H cells, AF mainly induced large-scale DNA damage and replication stress, leading to the induction of apoptotic cell death rather than ferroptosis. Importantly, all cell death types were immunogenic since the release of danger signals (ecto-calreticulin, ATP and HMGB1) and dendritic cell maturation occurred irrespective of (mutant) p53 expression. Finally, we show that AF sensitized cancer cells to caspase-independent natural killer cell-mediated killing by downregulation of several key targets of GZMA. Our data provides novel insights on AF as a potent, clinically available, off-patent cancer drug by targeting mutant p53 cancer cells through distinct cell death mechanisms (apoptosis and ferroptosis). In addition, AF improves the innate immune response at both cytostatic (natural killer cell-mediated killing) and cytotoxic concentrations (dendritic cell maturation).
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