ArticleBritish journal of pharmacology2004
Auranofin induces apoptosis and when combined with retinoic acid enhances differentiation of acute promyelocytic leukaemia cells in vitro.
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
- Auranofin Synergizes with the PARP Inhibitor Olaparib to Induce ROS-Mediated Cell Death in Mutant p53 Cancers.Antioxidants (Basel, Switzerland) · 2023Article
- Upgrade of an old drug: Auranofin in innovative cancer therapies to overcome drug resistance and to increase drug effectiveness.Medicinal research reviews · 2022Review
- Deubiquitinases in hematological malignancies.Biomarker research · 2021Review
- Auranofin, a thioredoxin reductase inhibitor, causes platelet death through calcium overload.Platelets · 2019Article
- An Overview of the Synthesis of Gold Nanoparticles Using Radiation Technologies.Nanomaterials (Basel, Switzerland) · 2018Review
- Article
- Peroxiredoxin Involvement in the Initiation and Progression of Human Cancer.Antioxidants & redox signaling · 2018Review
- Dual targeting of the thioredoxin and glutathione systems in cancer and HIV.The Journal of clinical investigation · 2016Review
- Gold(I) NHC-based homo- and heterobimetallic complexes: synthesis, characterization and evaluation as potential anticancer agents.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2015Article
- Article
- Article
- Auranofin displays anticancer activity against ovarian cancer cells through FOXO3 activation independent of p53.International journal of oncology · 2014Article
- A candidate anti-HIV reservoir compound, auranofin, exerts a selective 'anti-memory' effect by exploiting the baseline oxidative status of lymphocytes.Cell death & disease · 2013Article
- Antiproliferative effect of gold(I) compound auranofin through inhibition of STAT3 and telomerase activity in MDA-MB 231 human breast cancer cells.BMB reports · 2013Article
- The biological activity of auranofin: implications for novel treatment of diseases.Inflammopharmacology · 2012Review
- Effect of ascorbic acid on reactive oxygen species production in chemotherapy and hyperthermia in prostate cancer cells.The journal of physiological sciences : JPS · 2012Article
- Colorectal cancer and NF-κB signaling pathway.Gastroenterology and hepatology from bed to bench · 2011Article
- The tumor proteasome as a novel target for gold(III) complexes: implications for breast cancer therapy.Coordination chemistry reviews · 2009Article
- Arsenic trioxide and auranofin inhibit selenoprotein synthesis: implications for chemotherapy for acute promyelocytic leukaemia.British journal of pharmacology · 2008Article
- Auranofin promotes retinoic acid- or dihydroxyvitamin D3-mediated cell differentiation of promyelocytic leukaemia cells by increasing histone acetylation.British journal of pharmacology · 2008Article
Corrections and comments
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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
1. Acute promyelocytic leukaemia (APL) is characterized by a block in differentiation at the promyelocyte stage. Here, we describe the effects of auranofin (AF), a coordinated gold compound, on apoptosis and differentiation of APL cells. 2. Nucleosomal DNA fragmentation assay and Hoechst 33342 staining indicated that AF induced apoptosis in APL-derived NB4 cells at low concentrations (0.5-1.0 microm). The AF-induced apoptosis involved caspase-3 activation and specific cleavage of poly-ADP-ribose polymerase. 3. The AF-treated NB4 cells also produced reactive oxygen species (ROS) and cotreatment with N-acetyl-l-cysteine protected the NB4 cells from AF-induced apoptosis. 4. Expression of the CD11b cell surface marker and C/EBPepsilon was increased when the cells were treated for 4 days with 0.3 microm AF and a physiological concentration of all-trans retinoic acid (ATRA, 5 nm). Treatment with AF in combination with ATRA markedly increased the number of cells with differentiated features, such as lobed or multiple nuclei and numerous granules and vacuoles. At these low concentrations, neither AF nor ATRA alone induced significant cell differentiation. 5. These findings suggest not only that AF induces caspase-3-dependent apoptosis via a mechanism involving ROS, but also that the combined treatment with AF and ATRA induces differentiation of NB4 cells. Our results demonstrate a novel characteristic of AF from which an effective drug treatment of APL might be developed.
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