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Noncoding RNA transcription at enhancers and genome folding in cancer

机译:癌症中增强子的非编码RNA转录和基因组折叠

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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.
机译:将谱系特异性基因的核定位从转录惰性转变为宽松的环境,是确定细胞身份的关键步骤。已在多种细胞类型中发现了非编码RNA转录介导的基因组折叠和靶基因表达的激活。超级增强子的非编码RNA ThymoD(胸腺细胞分化因子)转录对于小鼠T细胞谱系承诺至关重要。 ThymoD转录的停止消除了转录介导的去甲基化作用,募集了诸如粘着蛋白复合物,CCCTC结合因子(CTCF)之类的循环因子,最终导致了严重的联合免疫缺陷和T细胞白血病/淋巴瘤的表型。在这篇综述中,我们描述了RNA聚合酶II介导的转录在增强子和基因组折叠中的功能作用。我们还强调了癌症发展中错误激活或抑制增强子转录和增强子-启动子相互作用的情况。

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