Journal
BIOMOLECULES
Volume 11, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/biom11020143
Keywords
H3K4 trimethylation; DNA hypermethylation; acute myeloid leukemia; cancer
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Funding
- University of Rome Sapienza [C26A15S3JR]
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CpG methylation plays vital roles in gene regulation, with CpG islands in promoters remaining unmethylated throughout mammalian embryogenesis and development. Understanding the mechanisms and effects of aberrant CpG island hypermethylation in tumors requires further investigation.
CpG methylation in transposons, exons, introns and intergenic regions is important for long-term silencing, silencing of parasitic sequences and alternative promoters, regulating imprinted gene expression and determining X chromosome inactivation. Promoter CpG islands, although rich in CpG dinucleotides, are unmethylated and remain so during all phases of mammalian embryogenesis and development, except in specific cases. The biological mechanisms that contribute to the maintenance of the unmethylated state of CpG islands remain elusive, but the modification of established DNA methylation patterns is a common feature in all types of tumors and is considered as an event that intrinsically, or in association with genetic lesions, feeds carcinogenesis. In this review, we focus on the latest results describing the role that the levels of H3K4 trimethylation may have in determining the aberrant hypermethylation of CpG islands in tumors.
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