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The role of epigenetic transcription repression and DNA methyltransferases in cancer
Author(s) -
Daniel Filipe Ivan,
Cherubini Karen,
Yurgel Liliane Soares,
de Figueiredo Maria Antonia Zancanaro,
Salum Fernanda Gonçalves
Publication year - 2010
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/cncr.25482
Subject(s) - cancer epigenetics , methyltransferase , epigenetics of physical exercise , dna methylation , epigenetics , epigenomics , biology , transcription (linguistics) , methylation , cpg site , cancer research , histone methylation , psychological repression , histone methyltransferase , genetics , dna , gene , gene expression , linguistics , philosophy
Epigenetic alterations such as DNA methylation have been implicated in the development and progression of various cancers. DNA methylation consists of the reversible addition of a methyl group to the carbon 5 position of cytosine in CpG dinucleotides and is considered essential for normal embryonic development. However, global genomic hypomethylation and aberrant hypermethylation of regulatory regions of tumor suppressor genes have been associated with chromosomal instability and transcription repression, respectively, providing neoplastic cells with a selective advantage. DNA methyltransferases are the enzymes responsible for the addition of methyl groups to CpG dinucleotides, which, together with histone modifiers, initiate the events necessary for transcription repression to occur. It has been demonstrated that increased expression of DNA methyltransferases may contribute to tumor progression through methylation‐mediated gene inactivation in various human cancers. Given their importance, this article reviews the main epigenetic mechanisms for regulating transcription and its implications in cancer development. Cancer 2011. © 2010 American Cancer Society.