The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.
NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink
Open accessAbstract
Nicotinamide N-methyltransferase (NNMT) is overexpressed in a variety of human cancers, where it contributes to tumorigenesis by a still poorly understood mechanism. Here, we show using metabolomics that NNMT impairs the methylation potential of cancer cells by consuming methyl units from S-adenosyl methionine to create the stable metabolic product 1-methylnicotinamide. As a result, NNMT-expressing cancer cells possess an altered epigenetic state that includes hypomethylated histones and other cancer-related proteins combined with heightened expression of pro-tumorigenic gene products. Our findings thus point to a direct mechanistic link between the deregulation of a metabolic enzyme and widespread changes in the methylation landscape of cancer cells.
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Akt-dependent metabolic reprogramming regulates tumor cell histone acetylation
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Metadata
- Authors
- Ulanovskaya, O. A., Zuhl, A. M., & Cravatt, B. F.
- Venue
- Nature Chemical Biology
- Published
- 2013-03-03
- Volume
- 9
- Issue
- 5
- Pages
- 300-306
- ISSN
- 1552-4450 (ISSN-L)
- 1552-4469
- OpenAlex
- W2101045506
- Cited by
- 447
- References
- 54
- FWCI
- 7.93
- Type
- journal article
- Language
- en
- Open access
- green
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- Ulanovskaya, O. A., Zuhl, A. M., & Cravatt, B. F. (2013). NNMT promotes epigenetic remodeling in cancer by creating a metabolic methylation sink. Nature Chemical Biology. https://doi.org/10.1038/nchembio.1204
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
