Bookmarking target genes in mitosis: a shared epigenetic trait of phenotypic transcription factors and oncogenes?
Bookmarking target genes in mitosis: a shared epigenetic trait of phenotypic transcription factors and oncogenes?
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有丝分裂中的目标基因书签：表型转录因子和癌基因的共同表观遗传特征？
DOI：
10.1158/0008-5472.can-13-2837
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发表时间：
2014
期刊：
影响因子：
11.2
通讯作者：
Stein,GaryS
中科院分区：
文献类型：
--
作者：
Zaidi,SayyedK;Grandy,RodrigoA;Lopez-Camacho,Cesar;Montecino,Martin;vanWijnen,AndreJ;Lian,JaneB;Stein,JanetL;Stein,GaryS
正常细胞和肿瘤细胞的表型、增殖和生长的调控信息必须通过 S 期的基因组复制和有丝分裂期间的细胞分裂来维持。表观遗传机制包括 DNA 甲基化、组蛋白翻译后修饰、组蛋白变体的选择性利用和可遗传的 RNA 分子，在通过有丝分裂维持细胞身份方面发挥着关键作用。最近的研究表明，谱系限制性转录因子对基因的有丝分裂占据是细胞命运、生长和增殖的决定因素，是细胞表达记忆保留和传递的关键表观遗传机制。越来越多的证据表明，有丝分裂染色体中存在独特的转录调控微环境，其中有丝分裂后重新激活的基因。重要的是，一些癌蛋白存在于有丝分裂微环境中，它们在有丝分裂过程中占据靶基因，并可能有助于维持转化的表型。我们讨论了有丝分裂过程中表观遗传学标记基因对生理控制以及癌症发生和进展的新兴调控影响。 74(2)； 420–5。 ©2014 AACR。
The regulatory information for phenotype, proliferation, and growth of normal and tumor cells must be maintained through genome replication in the S phase and cell division during mitosis. Epigenetic mechanisms that include DNA methylation, posttranslational modifications of histones, selective utilization of histone variants, and inheritable RNA molecules play pivotal roles in maintaining cellular identity through mitotic divisions. Recent studies demonstrate that mitotic occupancy of genes, which are determinants of cell fate, growth, and proliferation, by lineage-restricted transcription factors is a key epigenetic mechanism for retention and transmission of cellular expression memory. Evidence is emerging for the presence of distinct transcriptional regulatory microenvironments in mitotic chromosomes in which the genes bookmarked for reactivation postmitotically reside. Importantly, some oncoproteins are present in mitotic microenvironments where they occupy target genes during mitosis and may contribute to perpetuating the transformed phenotype. We discuss emerging regulatory implications of epigenetically bookmarking genes during mitosis for physiologic control as well as for the onset and progression of cancer.Cancer Res; 74(2); 420–5. ©2014 AACR.