ArticleNature communications2025
Nitric oxide inhibits ten-eleven translocation DNA demethylases to regulate 5mC and 5hmC across the genome.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed.
- Article
- Nitric oxide dependent metabolic and genetic dysregulation in metastatic triple-negative breast cancer.The Journal of biological chemistry · 2026Article
- Nitric oxide-driven Warburg reprogramming at the NOS2-COX2 axis: An integrative engine of cancer hallmarks.Redox biology · 2026Review
- Recent Advances in Genetically Engineered Mouse Models of Melanoma: Insights into Tumor Initiation and Oncogenic Signaling Pathways.International journal of stem cells · 2026Review
- Combined epigenomic landscapes of 5mC, 5hmC, and 6mA modifications in papillary thyroid carcinogenesis.Communications biology · 2026Article
- Article
- Article
- How chronic inflammation fuels carcinogenesis as an environmental epimutagen.Discover oncology · 2025Review
- Real-time nitric oxide detection in cytokine stimulated cancer cells and macrophages.Nitric oxide : biology and chemistry · 2025Article
- Review
- TET1-mediated DNA demethylation suppresses migration of goat placental trophoblast cells.Journal of animal science · 2025Article
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21 authors.
Funding
Abstract
DNA methylation at cytosine bases (5-methylcytosine, 5mC) is a heritable epigenetic mark regulating gene expression. While enzymes that metabolize 5mC are well-characterized, endogenous signaling molecules that regulate DNA methylation machinery have not been described. We report that physiological nitric oxide (NO) concentrations reversibly inhibit the DNA demethylases TET and ALKBH2 by binding to the mononuclear non-heme iron atom forming a dinitrosyliron complex (DNIC) and preventing cosubstrates from binding. In cancer cells treated with exogenous NO, or endogenously synthesizing NO, 5mC and 5-hydroxymethylcytosine (5hmC) increase, with no changes in DNA methyltransferase activity. 5mC is also significantly increased in NO-producing patient-derived xenograft tumors from mice. Genome-wide methylome analysis of cells chronically treated with NO (10 days) shows enrichment of 5mC and 5hmC at gene-regulatory loci, correlating with altered expression of NO-regulated tumor-associated genes. Regulation of DNA methylation is distinctly different from canonical NO signaling and represents a unique epigenetic role for NO.
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