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MCM3AP-AS1/miR-211/KLF5/AGGF1轴调控胶质母细胞瘤血管生成的作用

The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis.

作者信息

Yang Chunqing, Zheng Jian, Xue Yixue, Yu Hai, Liu Xiaobai, Ma Jun, Liu Libo, Wang Ping, Li Zhen, Cai Heng, Liu Yunhui

机构信息

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

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

出版信息

Front Mol Neurosci. 2018 Jan 9;10:437. doi: 10.3389/fnmol.2017.00437. eCollection 2017.

DOI:10.3389/fnmol.2017.00437
PMID:29375300
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5767169/
Abstract

Glioblastoma (GBM) is the most aggressive and malignant primary tumor. Angiogenesis plays a critical role in the progression of GBM. Previous studies have indicated that long non-coding RNAs (lncRNAs) are abnormally expressed in various cancers and participate in the regulation of the malignant behaviors of tumors. The present study demonstrated that lncRNA antisense 1 to Micro-chromosome maintenance protein 3-associated protein (MCM3AP-AS1) was upregulated whereas miR-211 was downregulated in glioma-associated endothelial cells (GECs). Knockdown of MCM3AP-AS1 suppressed the cell viability, migration, and tube formation of GECs and played a role in inhibiting angiogenesis of GBM . Furthermore, knockdown of MCM3AP-AS1 increased the expression of miR-211. Luciferase reporter assay implicated that miR-211 targeted KLF5 3'-UTR and consequently inhibited KLF5 expression. Besides, in this study we found that MCM3AP-AS1 knockdown decreased KLF5 and AGGF1 expression by upregulating miR-211. In addition, KLF5 was associated with the promoter region of AGGF1. Knockdown of KLF5 decreased AGGF1 expression by transcriptional repression, and also inhibited the activation of PI3K/AKT and ERK1/2 signaling pathways. Overall, this study reveals that MCM3AP-AS1/miR-211/KLF5/AGGF1 axis plays a prominent role in the regulation of GBM angiogenesis and also serves as new therapeutic target for the anti-angiogenic therapy of glioma.

摘要

胶质母细胞瘤（GBM）是最具侵袭性和恶性的原发性肿瘤。血管生成在GBM的进展中起着关键作用。先前的研究表明，长链非编码RNA（lncRNAs）在各种癌症中异常表达，并参与肿瘤恶性行为的调控。本研究表明，在胶质瘤相关内皮细胞（GECs）中，微小染色体维持蛋白3相关蛋白反义1（MCM3AP-AS1）上调，而miR-211下调。敲低MCM3AP-AS1可抑制GECs的细胞活力、迁移和管腔形成，并在抑制GBM血管生成中发挥作用。此外，敲低MCM3AP-AS1可增加miR-211的表达。荧光素酶报告基因检测表明，miR-211靶向KLF5的3'-UTR，从而抑制KLF5的表达。此外，在本研究中我们发现，敲低MCM3AP-AS1通过上调miR-211降低KLF5和AGGF1的表达。此外，KLF5与AGGF1的启动子区域相关。敲低KLF5通过转录抑制降低AGGF1的表达，同时也抑制PI3K/AKT和ERK1/2信号通路的激活。总体而言，本研究揭示了MCM3AP-AS1/miR-211/KLF5/AGGF1轴在GBM血管生成调控中起重要作用，也为胶质瘤的抗血管生成治疗提供了新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d2f/5767169/1973e386cc7e/fnmol-10-00437-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d2f/5767169/f6ebc8e2913d/fnmol-10-00437-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d2f/5767169/1973e386cc7e/fnmol-10-00437-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d2f/5767169/ec5e70135c9a/fnmol-10-00437-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d2f/5767169/0891fb075bf6/fnmol-10-00437-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d2f/5767169/776d4c6a2fe5/fnmol-10-00437-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d2f/5767169/1973e386cc7e/fnmol-10-00437-g008.jpg

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