Journal
MOLECULAR ONCOLOGY
Volume 6, Issue 6, Pages 567-578Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.molonc.2012.07.007
Keywords
MicroRNA; DNA methylation; Epigenetic silencing; Tumor suppressor
Categories
Funding
- Japan Society for Promotion of Science
- Ministry of Health, Labor, and Welfare, Japan
- A3 Foresight Program from the Japan Society for Promotion of Science
- Grants-in-Aid for Scientific Research [22790655, 23501261] Funding Source: KAKEN
Ask authors/readers for more resources
DNA methylation plays a key role in the silencing of numerous cancer-related genes, thereby affecting a number of vital cellular processes, including the cell cycle checkpoint, apoptosis, signal transduction, cell adhesion and angiogenesis. Also widely altered in human malignancies is the expression of microRNAs (miRNAs), a class of small noncoding RNAs that act as posttranscriptional regulators of gene expression. Furthermore, emerging evidence now supports the idea that DNA methylation is crucially involved in the dysregulation of miRNAs in cancer. This is in part the result of technological advances that enable more comprehensive analysis of miRNA expression profiles and the epigenome in cancer cells, which has led to the identification of a number of epigenetically regulated miRNAs. As with protein-coding genes, it appears that miRNA genes involved in regulating cancer-related pathways are silenced in association with CpG island hypermethylation. In addition, methylation in CpG island shore regions and DNA hypomethylation also appear to contribute to miRNA dysregulation in cancer. Aberrant DNA methylation of miRNA genes is a potentially useful biomarker for detecting cancer and predicting its outcome. Moreover, re-expression of miRNAs and the replacement of tumor suppressive miRNAs using miRNA mimics or expression vectors could be effective approaches to cancer therapy. (c) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available