EZH2 Methyltransferase and H3K27 Methylation in Breast Cancer

被引:234
作者
Yoo, Kyung Hyun [1 ]
Hennighausen, Lothar [1 ]
机构
[1] NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA
关键词
EZH2; H3K27; methylation; Breast cancer; BRCA1; EMBRYONIC STEM-CELLS; HISTONE METHYLTRANSFERASE; DEVELOPMENTAL REGULATORS; POLYCOMB; EXPRESSION; H3; MECHANISMS; CARCINOMA; COMPLEX; PROTEIN;
D O I
10.7150/ijbs.8.59
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Histone modifications are thought to control the regulation of genetic programs in normal physiology and cancer. Methylation (mono-, di-, and tri-methylation) on histone H3 lysine (K) 27 induces transcriptional repression, and thereby participates in controlling gene expression patterns. Enhancer of zeste (EZH) 2, a methyltransferase and component of the polycomb repressive complex 2 (PRC2), plays an essential role in the epigenetic maintenance of the H3K27me3 repressive chromatin mark. Abnormal EZH2 expression has been associated with various cancers including breast cancer. Here, we discuss the contribution of EZH2 and the PRC2 complex in controlling the H3K27 methylation status and subsequent consequences on genomic instability and the cell cycle in breast cancer cells. We also discuss distinct molecular mechanisms used by EZH2 to suppress BRCA1 functions.
引用
收藏
页码:59 / 65
页数:7
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