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上游开放阅读框通过 ZNRD1-AS1/miR-499a-5p/ELF1/EMI1 通路调控胶质瘤血管生成拟态。

An upstream open reading frame regulates vasculogenic mimicry of glioma via ZNRD1-AS1/miR-499a-5p/ELF1/EMI1 pathway.

机构信息

Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang, China.

Liaoning Clinical Medical Research Center in Nervous System Disease, Shenyang, China.

出版信息

J Cell Mol Med. 2020 Jun;24(11):6120-6136. doi: 10.1111/jcmm.15217. Epub 2020 May 5.

DOI:10.1111/jcmm.15217
PMID:32368853
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7294115/
Abstract

Increasing evidence has suggested that gliomas can supply blood through vasculogenic mimicry. In this study, the expression and function of ZNRD1-AS1-144aa-uORF (144aa-uORF) and some non-coding RNAs in gliomas were assessed. Real-time quantitative PCR or Western blot was used to discover the expression of 144aa-uORF, ZNRD1-AS1, miR-499a-5p, ELF1 and EMI1 in gliomas. In addition, RIP and RNA pull-down assays were applied to explore the interrelationship between 144aa-uORF and ZNRD1-AS1. The role of the 144aa-uORF\ZNRD1-AS1\miR-499a-5p\ELF1\EMI1 axis in vasculogenic mimicry formation of gliomas was analysed. This study illustrates the reduced expression of the 144aa-uORF in glioma tissues and cells. Up-regulation of 144aa-uORF inhibits proliferation, migration, invasion and vasculogenic mimicry formation within glioma cells. The up-regulated 144aa-uORF can increase the degradation of ZNRD1-AS1 through the nonsense-mediated RNA decay (NMD) pathway. Knockdown of ZNRD1-AS1 inhibits vasculogenic mimicry in glioma cells by modulating miR-499a-5p. At the same time, miR-499a-5p is down-regulated and has a tumour-suppressive effect in gliomas. In addition, ZNRD1-AS1 serves as a competitive endogenous RNA (ceRNA) and regulates the expression of ELF1 by binding to miR-499a-5p. Notably, ELF1 binds to the promoter region of EMI1 and up-regulates EMI1 expression, while simultaneously promoting vasculogenic mimicry in glioma cells. This study suggests that the 144aa-uORF\ZNRD1-AS1\miR-499a-5p\ELF1\EMI1 axis takes key part in regulating the formation of vasculogenic mimicry in gliomas and may provide a potential target for glioma treatment.

摘要

越来越多的证据表明，神经胶质瘤可以通过血管生成拟态来提供血液。在这项研究中，评估了神经胶质瘤中 ZNRD1-AS1-144aa-uORF（144aa-uORF）和一些非编码 RNA 的表达和功能。实时定量 PCR 或 Western blot 用于发现神经胶质瘤中 144aa-uORF、ZNRD1-AS1、miR-499a-5p、ELF1 和 EMI1 的表达。此外，还应用 RIP 和 RNA 下拉测定来探讨 144aa-uORF 和 ZNRD1-AS1 之间的相互关系。分析了 144aa-uORF\ZNRD1-AS1\miR-499a-5p\ELF1\EMI1 轴在神经胶质瘤血管生成拟态形成中的作用。本研究说明了神经胶质瘤组织和细胞中 144aa-uORF 的表达减少。上调 144aa-uORF 抑制神经胶质瘤细胞的增殖、迁移、侵袭和血管生成拟态形成。上调的 144aa-uORF 通过无意义介导的 RNA 降解（NMD）途径增加 ZNRD1-AS1 的降解。ZNRD1-AS1 的敲低通过调节 miR-499a-5p 抑制神经胶质瘤细胞中的血管生成拟态。同时，miR-499a-5p 在神经胶质瘤中下调并具有肿瘤抑制作用。此外，ZNRD1-AS1 作为竞争性内源性 RNA（ceRNA），通过与 miR-499a-5p 结合来调节 ELF1 的表达。值得注意的是，ELF1 结合到 EMI1 的启动子区域并上调 EMI1 表达，同时促进神经胶质瘤细胞中的血管生成拟态。本研究表明，144aa-uORF\ZNRD1-AS1\miR-499a-5p\ELF1\EMI1 轴在调节神经胶质瘤血管生成拟态形成中起着关键作用，可能为神经胶质瘤的治疗提供一个潜在的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26ac/7294115/949f49cafc07/JCMM-24-6120-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26ac/7294115/949f49cafc07/JCMM-24-6120-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26ac/7294115/de390f4e43af/JCMM-24-6120-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26ac/7294115/cba17d9e880a/JCMM-24-6120-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26ac/7294115/399012e13d75/JCMM-24-6120-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26ac/7294115/f5870514e499/JCMM-24-6120-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26ac/7294115/949f49cafc07/JCMM-24-6120-g007.jpg

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