Wang Gang G, Allis C David, Chi Ping
Laboratory of Chromatin Biology, The Rockefeller University, and Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.
Trends Mol Med. 2007 Sep;13(9):373-80. doi: 10.1016/j.molmed.2007.07.004. Epub 2007 Sep 5.
Connections between perturbations that lie outside of our genome, that is, epigenetic alternations, and tumorigenesis have become increasingly apparent. Dynamic chromatin remodeling of the fundamental nucleosomal structure (covered in this review) or the covalent marks residing in the histone proteins that make up this structure (covered previously in part I) underlie many fundamental cellular processes, including transcriptional regulation and DNA-damage repair. Dysregulation of these processes has been linked to cancer development. Mechanisms of chromatin remodeling include dynamic interplay between ATP-dependent complexes, covalent histone modifications, utilization of histone variants and DNA methylation. In part II of this series, we focus on connections between ATP-dependent chromatin-remodeling complexes and oncogenesis and discuss the potential clinical implications of chromatin remodeling and cancer.
我们基因组之外的扰动（即表观遗传改变）与肿瘤发生之间的联系已变得越来越明显。基本核小体结构的动态染色质重塑（本综述涵盖）或构成该结构的组蛋白上的共价标记（先前在第一部分中涵盖）是许多基本细胞过程的基础，包括转录调控和DNA损伤修复。这些过程的失调与癌症发展有关。染色质重塑机制包括ATP依赖复合物之间的动态相互作用、组蛋白共价修饰、组蛋白变体的利用和DNA甲基化。在本系列的第二部分中，我们重点关注ATP依赖的染色质重塑复合物与肿瘤发生之间的联系，并讨论染色质重塑与癌症的潜在临床意义。
