Journal
NATURE CHEMICAL BIOLOGY
Volume 9, Issue 5, Pages 300-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/NCHEMBIO.1204
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Funding
- NCI NIH HHS [CA132630, R01 CA132630] Funding Source: Medline
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Nicotinamide N-methyltransferase (NNMT) is overexpressed in a variety of human cancers, where it contributes to tumorigenesis by a mechanism that is still poorly understood. 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 have an altered epigenetic state that includes hypomethylated histones and other cancer-related proteins combined with heightened expression of protumorigenic 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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