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非编码RNA在先天性巨结肠症中的作用。

The roles of non-coding RNAs in Hirschsprung's disease.

作者信息

Yang Yang, Hou Xinwei, Wang Chen, Chen Qinming, Lu Yi, Yu Daiyue, Wu Kai

机构信息

Department of Pediatric Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, 510282, Guangdong, China.

出版信息

Noncoding RNA Res. 2024 Feb 28;9(3):704-714. doi: 10.1016/j.ncrna.2024.02.015. eCollection 2024 Sep.

DOI:10.1016/j.ncrna.2024.02.015
PMID:38577013
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10990754/
Abstract

Hirschsprung's disease (HSCR) is a congenital disorder characterized by the absence of ganglion cells in the colon, leading to various intestinal complications. The etiology of HSCR stems from complex genetic and environmental interactions, of which the intricate roles of non-coding RNAs (ncRNAs) are a key area of research. However, the roles of ncRNAs in the pathogenesis of HSCR have not been fully elucidated. In order to understand the variety of symptoms caused by HSCR and develop new therapeutic approaches, it is essential to understand the underlying biological genetic basis of HSCR. This review presents a comprehensive overview of the current understanding regarding the involvement of ncRNAs in HSCR, including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs). Additionally, it provides a summary of the molecular mechanisms through which ncRNAs regulate the expression of genes related to the proliferation, migration, and differentiation of intestinal neural crest cells, thereby contributing to the advancement of HSCR research.

摘要

先天性巨结肠症(HSCR)是一种先天性疾病,其特征是结肠中缺乏神经节细胞,可导致各种肠道并发症。HSCR的病因源于复杂的基因与环境相互作用,其中非编码RNA(ncRNA)的复杂作用是一个关键研究领域。然而,ncRNA在HSCR发病机制中的作用尚未完全阐明。为了了解HSCR引起的各种症状并开发新的治疗方法,了解HSCR潜在的生物遗传基础至关重要。本综述全面概述了目前对ncRNA参与HSCR的理解,包括微小RNA(miRNA)、长链非编码RNA(lncRNA)和环状RNA(circRNA)。此外,还总结了ncRNA调节与肠神经嵴细胞增殖、迁移和分化相关基因表达的分子机制,从而推动HSCR研究的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8048/10990754/ff45b2adc45f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8048/10990754/21c093d0d3a8/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8048/10990754/a33cb00b61f9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8048/10990754/ff45b2adc45f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8048/10990754/21c093d0d3a8/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8048/10990754/a33cb00b61f9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8048/10990754/ff45b2adc45f/gr3.jpg

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本文引用的文献

1
Circular RNA MTCL1 targets SMAD3 by sponging miR-145-5p for regulation of cell proliferation and migration in Hirschsprung's disease.环状 RNA MTCL1 通过海绵吸附 miR-145-5p 靶向 SMAD3 调控先天性巨结肠病细胞增殖和迁移。
Pediatr Surg Int. 2023 Dec 21;40(1):25. doi: 10.1007/s00383-023-05621-9.
2
Downregulation of miR-144 blocked the proliferation and invasion of nerve cells in Hirschsprung disease by regulating Transcription Factor AP 4 (TFAP4).下调 miR-144 通过调节转录因子 AP-4(TFAP4)阻断了先天性巨结肠症神经细胞的增殖和侵袭。
Pediatr Surg Int. 2023 Aug 23;39(1):251. doi: 10.1007/s00383-023-05530-x.
3
Identifying the potential transcriptional regulatory network in Hirschsprung disease by integrated analysis of microarray datasets.
通过微阵列数据集的综合分析鉴定先天性巨结肠症潜在的转录调控网络。
World J Pediatr Surg. 2023 Apr 17;6(2):e000547. doi: 10.1136/wjps-2022-000547. eCollection 2023.
4
Transcriptomics of Hirschsprung disease patient-derived enteric neural crest cells reveals a role for oxidative phosphorylation.遗传性巨结肠症患者来源的肠神经嵴细胞转录组学研究揭示了氧化磷酸化的作用。
Nat Commun. 2023 Apr 15;14(1):2157. doi: 10.1038/s41467-023-37928-5.
5
Up-Regulation of microRNA-424 Causes an Imbalance in AKT Phosphorylation and Impairs Enteric Neural Crest Cell Migration in Hirschsprung Disease.微小 RNA-424 的上调导致 AKT 磷酸化失衡,损害先天性巨结肠症中的肠神经嵴细胞迁移。
Int J Mol Sci. 2023 Apr 4;24(7):6700. doi: 10.3390/ijms24076700.
6
Update on the Pathogenesis of the Hirschsprung-Associated Enterocolitis.先天性巨结肠相关性结肠炎发病机制的研究进展。
Int J Mol Sci. 2023 Feb 27;24(5):4602. doi: 10.3390/ijms24054602.
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The Tumorigenic Effect of lncRNA AFAP1-AS1 is Mediated by Translated Peptide ATMLP Under the Control of m A Methylation.m⁶A 甲基化调控翻译肽 ATMLP 介导长链非编码 RNA AFAP1-AS1 促肿瘤活性
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Pediatr Surg Int. 2023 Feb 15;39(1):126. doi: 10.1007/s00383-023-05421-1.
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Clin Transl Med. 2023 Feb;13(2):e1193. doi: 10.1002/ctm2.1193.
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