Throwing the cancer switch: reciprocal roles of polycomb and trithorax proteins

被引:192
作者
Mills, Alea A. [1 ]
机构
[1] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
关键词
TUMOR-SUPPRESSOR GENE; MIXED-LINEAGE LEUKEMIA; CHROMATIN-REMODELING FACTOR; CELL-CYCLE PROGRESSION; COVALENT HISTONE MODIFICATIONS; DEMETHYLASE JMJD3 CONTRIBUTES; ENDOCRINE NEOPLASIA TYPE-2; AGGRESSIVE BREAST-CANCER; MYC TRANSGENIC MICE; CHROMOSOME ARM 1P;
D O I
10.1038/nrc2931
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The discovery that cancer can be governed above and beyond the level of our DNA presents a new era for designing therapies that reverse the epigenetic state of a tumour cell. Understanding how altered chromatin dynamics leads to malignancy is essential for controlling tumour cells while sparing normal cells. Polycomb and trithorax group proteins are evolutionarily conserved and maintain chromatin in the 'off' or 'on' states, thereby preventing or promoting gene expression, respectively. Recent work highlights the dynamic interplay between these opposing classes of proteins, providing new avenues for understanding how these epigenetic regulators function in tumorigenesis.
引用
收藏
页码:669 / 682
页数:14
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