ArticlePloS one2014
Targeting catalase but not peroxiredoxins enhances arsenic trioxide-induced apoptosis in K562 cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- The Mechanism of Anti-Tumor Activity of 6-Morpholino- and 6-Amino-9-Sulfonylpurine Derivatives on Human Leukemia Cells.Molecules (Basel, Switzerland) · 2023Article
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Relationship between Oxidative Stress and Imatinib Resistance in Model Chronic Myeloid Leukemia Cells.Biomolecules · 2021Article
- Inhibition of red blood cell development by arsenic-induced disruption of GATA-1.Scientific reports · 2020Article
- Cellular and molecular alterations induced by low‑dose fisetin in human chronic myeloid leukemia cells.International journal of oncology · 2019Article
- Catalase S-Glutathionylation by NOX2 and Mitochondrial-Derived ROS Adversely Affects Mice and Human Neutrophil Survival.Inflammation · 2019Article
- Peroxisomal Hydrogen Peroxide Metabolism and Signaling in Health and Disease.International journal of molecular sciences · 2019Review
- Local Tumor Ischemia-Reperfusion Mediated By Ultrasound-Targeted Microbubble Destruction Enhances The Anti-Tumor Efficacy Of Doxorubicin Chemotherapy.Cancer management and research · 2019Article
- Catalase down-regulation in cancer cells exposed to arsenic trioxide is involved in their increased sensitivity to a pro-oxidant treatment.Cancer cell international · 2018Article
- Biochanin A Ameliorates Arsenic-Induced Hepato- and Hematotoxicity in Rats.Molecules (Basel, Switzerland) · 2016Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite considerable efficacy of arsenic trioxide (As2O3) in acute promyelocytic leukemia (APL) treatment, other non-APL leukemias, such as chronic myeloid leukemia (CML), are less sensitive to As2O3 treatment. However, the underlying mechanism is not well understood. Here we show that relative As2O3-resistant K562 cells have significantly lower ROS levels than As2O3-sensitive NB4 cells. We compared the expression of several antioxidant enzymes in these two cell lines and found that peroxiredoxin 1/2/6 and catalase are expressed at high levels in K562 cells. We further investigated the possible role of peroxirdoxin 1/2/6 and catalase in determining the cellular sensitivity to As2O3. Interestingly, knockdown of peroxiredoxin 1/2/6 did not increase the susceptibility of K562 cells to As2O3. On the contrary, knockdown of catalase markedly enhanced As2O3-induced apoptosis. In addition, we provide evidence that overexpression of BCR/ABL cannot increase the expression of PRDX 1/2/6 and catalase. The current study reveals that the functional role of antioxidant enzymes is cellular context and treatment agents dependent; targeting catalase may represent a novel strategy to improve the efficacy of As2O3 in CML treatment.
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