A DNA methylation signature associated with the epigenetic repression of glycine N-methyltransferase in human hepatocellular carcinoma View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2013-08

AUTHORS

Covadonga Huidobro, Estela G. Toraño, Agustín F. Fernández, Rocío G. Urdinguio, Ramón M. Rodríguez, Cecilia Ferrero, Pablo Martínez-Camblor, Loreto Boix, Jordi Bruix, Juan Luís García-Rodríguez, Marta Varela-Rey, José María Mato, María Luz Martínez-Chantar, Mario F. Fraga

ABSTRACT

The basic mechanisms underlying promoter DNA hypermethylation in cancer are still largely unknown. It has been proposed that the levels of the methyl donor group in DNA methylation reactions, S-adenosylmethionine (SAMe), might be involved. SAMe levels depend on the glycine-N-methyltransferase (GNMT), a one-carbon group methyltransferase, which catalyzes the conversion of SAMe to S-adenosylhomocysteine in hepatic cells. GNMT has been proposed to display tumor suppressor activity and to be frequently repressed in hepatocellular carcinoma (HCC). In this study, we show that GNMT shows aberrant DNA hypermethylation in some HCC cell lines and primary tumors (20 %). GNMT hypermethylation could contribute to gene repression and its restoration in cell lines displaying hypermethylation-reduced tumor growth in vitro. In agreement, human primary tumors expressing GNMT were of smaller size than tumors showing GNMT hypermethylation. Genome-wide analyses of gene promoter methylation identified 277 genes whose aberrant methylation in HCC was associated with GNMT methylation/expression. The findings in this manuscript indicate that DNA hypermethylation plays an important role in the repression of GNMT in HCC and that loss of GNMT in human HCC could promote the establishment of aberrant DNA methylation patterns at specific gene promoters. More... »

PAGES

939-950

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00109-013-1010-8

    DOI

    http://dx.doi.org/10.1007/s00109-013-1010-8

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1017799424

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/23475283


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