Epigenetic aberrations during oncogenesis

被引：127
作者：
Hatziapostolou, Maria [1 ,2 ]
Iliopoulos, Dimitrios [1 ,2 ]
机构：
[1] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA
[2] Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA
来源：
CELLULAR AND MOLECULAR LIFE SCIENCES | 2011年 / 68卷 / 10期
关键词：
Epigenetics; Networks; Methylation; Histones; MicroRNAs; Oncogenic transformation; HISTONE DEACETYLASE INHIBITORS; DEMETHYLASE JMJD3 CONTRIBUTES; CPG ISLAND HYPERMETHYLATION; PUTATIVE TUMOR-SUPPRESSOR; ACUTE MYELOID-LEUKEMIA; BINDING PROTEIN MECP2; DNA METHYLATION; CHROMOSOMAL INSTABILITY; PROMOTER METHYLATION; PROSTATE-CANCER;
D O I：
10.1007/s00018-010-0624-z
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The aberrant epigenetic landscape of a cancer cell is characterized by global genomic hypomethylation, CpG island promoter hypermethylation of tumor suppressor genes, and changes in histone modification patterns, as well as altered expression profiles of chromatin-modifying enzymes. Recent advances in the field of epigenetics have revealed that microRNAs' expression is also under epigenetic regulation and that certain microRNAs control elements of the epigenetic machinery. The reversibility of epigenetic marks catalyzed the development of epigenetic-altering drugs. However, a better understanding of the intertwined relationship between genetics, epigenetics and microRNAs is necessary in order to resolve how gene expression aberrations that contribute to tumorigenesis can be therapeutically corrected.
引用
收藏
页码：1681 / 1702
页数：22
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