ArticleThe Journal of biological chemistry2015
NADPH oxidase-generated hydrogen peroxide induces DNA damage in mutant FLT3-expressing leukemia cells.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 93 citations in OpenAlex.
- The Oxidative Stress: Origin and Role in Aging and Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- XOR-mediated tumor-selective nanomaterial therapy: achieving tumor and immune cell dual regulation through intracellular ROS generation.Journal of nanobiotechnology · 2026Article
- Iron: Regulation, redox homeostasis, and ferroptosis in cancer.Ferroptosis and oxidative stress · 2026Article
- Nicotinamide adenine dinucleotide phosphate oxidase 4 in lung disease: a review of its biology and therapeutic potential.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Hepatic Metabolic Dysregulation as a Potential Amplifier of Leukemogenesis Following mRNA Vaccination: A Novel Mechanistic Hypothesis.Medicina (Kaunas, Lithuania) · 2025Article
- Metabolic Signature ofJournal of personalized medicine · 2025Review
- Nanocomposite biosensor tracks honokiol-induced oxidative stress dynamics in 3D hydrogel-cultured lung cancer cells.Microsystems & nanoengineering · 2025Article
- Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- New Compounds with Enhanced Biological Activity Through the Strategic Introduction of Silylated Groups into Hydroxystearic Acids.Molecules (Basel, Switzerland) · 2025Article
- Preclinical activity of resazurin in acute myeloid leukaemia.British journal of haematology · 2025Article
- Where lung cancer and tuberculosis intersect: recent advances.Frontiers in immunology · 2025Review
- Ultra-fast genetically encoded sensor for precise real-time monitoring of physiological and pathophysiological peroxide dynamics.Research square · 2024Article
- The pleiotropic functions of reactive oxygen species in cancer.Nature cancer · 2024Review
- Structure-guided engineering of a fast genetically encoded sensor for real-time HbioRxiv : the preprint server for biology · 2024Article
- Connecting atrial fibrillation to digestive neoplasms: exploring mediation via ischemic stroke and heart failure in Mendelian randomization studies.Frontiers in oncology · 2024Article
- Reactive oxygen species and its role in pathogenesis and resistance to therapy in acute myeloid leukemia.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- RCCD1 promotes breast carcinogenesis through regulating hypoxia-associated mitochondrial homeostasis.Oncogene · 2023Article
- Article
- Iron-Dependent Cell Death: A New Treatment Approach against Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2023Review
- Chemical biology approaches to uncovering nuclear ROS control.Current opinion in chemical biology · 2023Review
2 more citing papers are in PubMed but not listed here.
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
Internal tandem duplication of the FMS-like tyrosine kinase (FLT3-ITD) receptor is present in 20% of acute myeloid leukemia (AML) patients and it has been associated with an aggressive AML phenotype. FLT3-ITD expressing cell lines have been shown to generate increased levels of reactive oxygen species (ROS) and DNA double strand breaks (DSBs). However, the molecular basis of how FLT3-ITD-driven ROS leads to the aggressive form of AML is not clearly understood. Our group has previously reported that inhibition of FLT3-ITD signaling results in post-translational down-regulation of p22(phox), a small membrane-bound subunit of the NADPH oxidase (NOX) complex. Here we demonstrated that 32D cells, a myeloblast-like cell line transfected with FLT3-ITD, have a higher protein level of p22(phox) and p22(phox)-interacting NOX isoforms than 32D cells transfected with the wild type FLT3 receptor (FLT3-WT). The inhibition of NOX proteins, p22(phox), and NOX protein knockdowns caused a reduction in ROS, as measured with a hydrogen peroxide (H2O2)-specific dye, peroxy orange 1 (PO1), and nuclear H2O2, as measured with nuclear peroxy emerald 1 (NucPE1). These reductions in the level of H2O2 following the NOX knockdowns were accompanied by a decrease in the number of DNA DSBs. We showed that 32D cells that express FLT3-ITD have a higher level of both oxidized DNA and DNA DSBs than their wild type counterparts. We also observed that NOX4 and p22(phox) localize to the nuclear membrane in MV4-11 cells expressing FLT3-ITD. Taken together these data indicate that NOX and p22(phox) mediate the ROS production from FLT3-ITD that signal to the nucleus causing genomic instability.
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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.