Mthfd1 is a modifier of chemically induced intestinal carcinogenesis
Carcinogenesis, ISSN: 1460-2180, Vol: 32, Issue: 3, Page: 427-433
2011
- 25Citations
- 20Captures
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Metrics Details
- Citations25
- Citation Indexes25
- 25
- CrossRef19
- Captures20
- Readers20
- 20
Article Description
The causal metabolic pathways underlying associations between folate and risk for colorectal cancer (CRC) have yet to be established. Folate-mediated one-carbon metabolism is required for the de novo synthesis of purines, thymidylate and methionine. Methionine is converted to S-adenosylmethionine (AdoMet), the major one-carbon donor for cellular methylation reactions. Impairments in folate metabolism can modify DNA synthesis, genomic stability and gene expression, characteristics associated with tumorigenesis. The Mthfd1 gene product, C1-tetrahydrofolate synthase, is a trifunctional enzyme that generates one-carbon substituted tetrahydrofolate cofactors for one-carbon metabolism. In this study, we use Mthfd1 mice, which demonstrate a 50% reduction in C1-tetrahydrofolate synthase, to determine its influence on tumor development in two mouse models of intestinal cancer, crosses between Mthfd1 and Apc mice and azoxymethane (AOM)-induced colon cancer in Mthfd1 mice. Mthfd1 hemizygosity did not affect colon tumor incidence, number or load in Apc mice. However, Mthfd1 deficiency increased tumor incidence 2.5-fold, tumor number 3.5-fold and tumor load 2-fold in AOM-treated mice. DNA uracil content in the colon was lower in Mthfd1 mice, indicating that thymidylate biosynthesis capacity does not play a significant role in AOM-induced colon tumorigenesis. Mthfd1 deficiency-modified cellular methylation potential, as indicated by the AdoMet: S-adenosylhomocysteine ratio and gene expression profiles, suggesting that changes in the transcriptome and/or decreased de novo purine biosynthesis and associated mutability cause cellular transformation in the AOM CRC model. This study emphasizes the impact and complexity of gene-nutrient interactions with respect to the relationships among folate metabolism and colon cancer initiation and progression. © The Author 2010. Published by Oxford University Press. All rights reserved.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=79952300119&origin=inward; http://dx.doi.org/10.1093/carcin/bgq270; http://www.ncbi.nlm.nih.gov/pubmed/21156972; https://academic.oup.com/carcin/article-lookup/doi/10.1093/carcin/bgq270; https://dx.doi.org/10.1093/carcin/bgq270; https://academic.oup.com/carcin/article-abstract/32/3/427/2463917?redirectedFrom=fulltext
Oxford University Press (OUP)
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