DNA methylation of tumor-suppressor miRNA genes in chronic lymphocytic leukemia

被引：21

作者：

Wang, Lu Qian ^{[1
]}

Chim, Chor Sang ^{[1
]}

机构：

[1] Univ Hong Kong, Queen Mary Hosp, Dept Med, Hong Kong, Hong Kong, Peoples R China

来源：

EPIGENOMICS | 2015年 / 7卷 / 03期

关键词：

chronic lymphocytic leukemia; DNA methylation; miRNAs; tumor suppressor; WNT SIGNALING PATHWAY; EPIGENETIC INACTIVATION; DOWN-REGULATION; GENOMIC ABERRATIONS; MICRORNA EXPRESSION; TCL1; EXPRESSION; NONCODING RNAS; CANCER; HYPERMETHYLATION; SURVIVAL;

D O I：

10.2217/epi.15.6

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

DNA methylation is one of the most important epigenetic modifications of the genome involved in the regulation of numerous cellular processes through gene silencing without altering DNA sequences. miRNAs, a class of single-stranded noncoding RNAs of 19-25 nucleotides in length, function as post-transcriptional regulators of gene expression leading to mRNA cleavage or translational repression of their corresponding target protein-coding genes. Recently, dysregulation of tumor suppressor miRNAs mediated by promoter DNA hypermethylation is implicated in human cancers, including B-cell chronic lymphocytic leukemia (CLL). Moreover, it appears that methylated miRNA genes could be potential biomarkers for CLL diagnosis or therapy. This review will highlight the role of aberrant methylation of miRNA genes in the pathogenesis of CLL.

引用

页码：461 / 473

页数：13

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