ArticleThe Journal of biological chemistry2009
Reactive oxygen species are not required for an arsenic trioxide-induced antioxidant response or apoptosis.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 43 citations in OpenAlex.
- N-Acetylcysteine Prevents Arsenic-Induced Apoptosis but Not Supernumerary Motor Neuron Development in Zebrafish Embryos: Assessment of Protein Carbonylation and the p53 Pathway.International journal of molecular sciences · 2026Article
- Arsenic trioxide and p97 inhibitor synergize against acute myeloid leukemia by targeting nascent polypeptides and activating the ZAKα-JNK pathway.Cancer gene therapy · 2024Article
- Nuclear Factor Erythroid 2-Related Factor 2 in Regulating Cancer Metabolism.Antioxidants & redox signaling · 2020Review
- Review
- Mitophagy, a potential therapeutic target for stroke.Journal of biomedical science · 2018Review
- Arsenic trioxide-mediated suppression of miR-182-5p is associated with potent anti-oxidant effects through up-regulation ofOncotarget · 2018Article
- Realgar nanoparticles versus ATO arsenic compounds induce in vitro and in vivo activity against multiple myeloma.British journal of haematology · 2017Article
- TrxR1 as a potent regulator of the Nrf2-Keap1 response system.Antioxidants & redox signaling · 2015Review
- Synthetic Lethal Approaches Exploiting DNA Damage in Aggressive Myeloma.Cancer discovery · 2015Article
- Retinoic acid synergizes ATO-mediated cytotoxicity by precluding Nrf2 activity in AML cells.British journal of cancer · 2014Article
- Downregulation of Mcl-1 through GSK-3β activation contributes to arsenic trioxide-induced apoptosis in acute myeloid leukemia cells.Leukemia · 2013Article
- Arsenic-mediated activation of the Nrf2-Keap1 antioxidant pathway.Journal of biochemical and molecular toxicology · 2013Review
- Activation of the Nrf2 pathway by inorganic arsenic in human hepatocytes and the role of transcriptional repressor Bach1.Oxidative medicine and cellular longevity · 2013Article
- Ethacrynic acid and a derivative enhance apoptosis in arsenic trioxide-treated myeloid leukemia and lymphoma cells: the role of glutathione S-transferase p1-1.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- Article
- Article
- Anticancer activity of metal complexes: involvement of redox processes.Antioxidants & redox signaling · 2011Review
- Chemistry of the cysteine sensors in Kelch-like ECH-associated protein 1.Antioxidants & redox signaling · 2010Review
- Arsenic trioxide downregulates specificity protein (Sp) transcription factors and inhibits bladder cancer cell and tumor growth.Experimental cell research · 2010Article
- Immunotoxicity and biodistribution analysis of arsenic trioxide in C57Bl/6 mice following a 2-week inhalation exposure.Toxicology and applied pharmacology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Arsenicals are both environmental carcinogens as well as therapeutic agents for the treatment of trypanosomiasis and more recently cancer. Arsenic trioxide (ATO) has been successfully used for the treatment of acute promyelocytic leukemia (APL) and has activity in multiple myeloma (MM). While signaling events associated with carcinogenesis have been well studied, it still remains to be determined which of these events are involved in anti-cancer signaling. To better define this response, gene expression profiling following ATO treatment of four MM cell lines was performed. The pattern was consistent with a strong antioxidative response, particularly of genes activated by Nrf2. While Nrf2 is expressed constitutively at the mRNA level, the protein is not detected in untreated cells. Consistent with inactivation of Keap1, Nrf2 protein is stabilized and present in the nucleus within 6 h of ATO treatment. Despite the activation of this antioxidative response, ROS may not be important in ATO-induced death. Inhibition of ATO-induced ROS with butylated hydroxyanisole (BHA) does not affect Nrf2 activation or cell death. Moreover, silencing Nrf2 had no effect on ATO-induced apoptosis. Together these data suggest that ROS is not important in the induction of the antioxidative response or cellular death by ATO.
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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.