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长链非编码RNA作为人类癌症中的一种表观遗传调节因子。

Long non-coding RNAs as an epigenetic regulator in human cancers.

作者信息

Kondo Yutaka, Shinjo Keiko, Katsushima Keisuke

机构信息

Division of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

出版信息

Cancer Sci. 2017 Oct;108(10):1927-1933. doi: 10.1111/cas.13342. Epub 2017 Aug 30.

DOI:10.1111/cas.13342
PMID:28776911
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5623749/
Abstract

Recent studies have described the important multiple roles of long non-coding RNAs (lncRNAs) during oncogenic transformation. Because the coding genome accounts for a small amount of total DNA, and many mutations leading to cancer occur in the non-coding genome, it is plausible that the dysregulation of such non-coding transcribes might also affect tumor phenotypes. Indeed, to date, lncRNAs have been reported to affect diverse biological processes through the regulation of mRNA stability, RNA splicing, chromatin structure, and miRNA-mediated gene regulation by acting as miRNA sponges. Furthermore, accumulating studies have described the roles of lncRNAs in tumorigenesis; however, the precise mechanisms of many lncRNAs are still under investigation. Here, we discuss recently reported mechanistic insights into how lncRNAs regulate gene expression and contribute to tumorigenesis through interactions with other regulatory molecules. We especially highlight the role of taurine upregulated gene 1, which was recently reported to have biological functions related to gene regulation, and discuss the future clinical implications of lncRNAs in cancer treatments.

摘要

近期研究已描述了长链非编码RNA(lncRNA)在致癌转化过程中的重要多重作用。由于编码基因组在总DNA中占比小,且许多导致癌症的突变发生在非编码基因组中,因此这类非编码转录物的失调也可能影响肿瘤表型,这是合理的。事实上,迄今为止,lncRNA已被报道可通过调节mRNA稳定性、RNA剪接、染色质结构以及作为miRNA海绵介导miRNA调控基因表达等方式,影响多种生物学过程。此外,越来越多的研究描述了lncRNA在肿瘤发生中的作用;然而,许多lncRNA的确切机制仍在研究中。在此,我们讨论近期报道的关于lncRNA如何通过与其他调控分子相互作用来调节基因表达并促进肿瘤发生的机制见解。我们特别强调了牛磺酸上调基因1的作用,该基因最近被报道具有与基因调控相关的生物学功能,并讨论了lncRNA在癌症治疗中的未来临床意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6b/5623749/b2a19044b9fc/CAS-108-1927-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6b/5623749/2579ecb393ca/CAS-108-1927-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6b/5623749/0d3c0ac6a42f/CAS-108-1927-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6b/5623749/b2a19044b9fc/CAS-108-1927-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6b/5623749/2579ecb393ca/CAS-108-1927-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6b/5623749/0d3c0ac6a42f/CAS-108-1927-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce6b/5623749/b2a19044b9fc/CAS-108-1927-g003.jpg

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PRC2 is dispensable for -mediated transcriptional repression.
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