Noncoding RNA transcription at enhancers and genome folding in cancer

被引:14
|
作者
Isoda, Takeshi [1 ]
Morio, Tomohiro [1 ]
Takagi, Masatoshi [1 ]
机构
[1] Tokyo Med & Dent Univ, Dept Pediat & Dev Biol, Tokyo, Japan
基金
日本学术振兴会;
关键词
cancer; genome folding; noncoding RNA; ThymoD; transcription; TERT PROMOTER MUTATIONS; LINEAGE COMMITMENT; ELONGATION COMPLEX; 3D GENOME; CHROMATIN; BINDING; COHESIN; ACTIVATION; REVEALS; SITES;
D O I
10.1111/cas.14107
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Changes of nuclear localization of lineage-specific genes from a transcriptionally inert to permissive environment are a crucial step in establishing the identity of a cell. Noncoding RNA transcription-mediated genome folding and activation of target gene expression have been found in a variety of cell types. Noncoding RNA ThymoD (thymocyte differentiation factor) transcription at superenhancers is essential for mouse T-cell lineage commitment. The cessation of ThymoD transcription abolishes transcription-mediated demethylation, recruiting looping factors such as the cohesin complex, CCCTC-binding factor (CTCF), ultimately leading to the phenotype of severe combined immunodeficiency and T-cell leukemia/lymphoma. In this review, we describe the functional role of RNA polymerase II-mediated transcription at enhancers and in genome folding. We also highlight the involvement of faulty activation or suppression of enhancer transcription and enhancer-promoter interaction in cancer development.
引用
收藏
页码:2328 / 2336
页数:9
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