MicroRNA-1298-3p inhibits proliferation and invasion of glioma cells by downregulating Nidogen-1

被引:23
|
作者
Xu, Xiaohe [1 ]
Ban, Yunchao [2 ]
Zhao, Zilong [2 ]
Pan, Qichen [2 ]
Zou, Jingyu [2 ]
机构
[1] China Med Univ, Dept Ophthalmol, Shengjing Hosp, Shenyang 110004, Liaoning, Peoples R China
[2] China Med Univ, Dept Neurosurg, Affiliated Hosp 1, Shenyang 110001, Liaoning, Peoples R China
来源
AGING-US | 2020年 / 12卷 / 09期
关键词
glioma; microRNA-1298-3p; NID1; apoptosis; METASTASIS; PROTEIN;
D O I
10.18632/aging.103087
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Glioma is the most prevalent tumor of the central nervous system. To identify differentially expressed miRNAs (DEMs) in gliomas of different grades, bioinformatics analysis was performed. The DEMs between low-grade gliomas (LGGs) and high-grade gliomas (HGGs) were identified by screening the Gene Expression Omnibus and The Cancer Genome Atlas databases using the LIMMA package. Six overlapping DEMs were identified by comparing LGGs and HGGs. Downregulation of miR-1298-3p correlated with poor overall survival rates in glioma patients. Overexpression of miR-1298-3p induced apoptosis of glioma cells and inhibited glioma cell proliferation, migration, and invasion. The basement membrane protein Nidogen-1 (NID1) was identified as a direct binding target of miR-1298-3p in glioma cells. MiR-1298-3p agonist downregulated the NID1 and vimentin levels, but upregulated the level of E-cadherin in glioma cells. Importantly, overexpression of miR-1298-3p induced apoptosis and reduced tumor growth in a mouse xenograft model of glioma. Our results show that miR-1298-3p functions as a tumor suppressor in glioma cells, and suggest that it might serve as a potential biomarker and therapeutic target in glioma patients.
引用
收藏
页码:7761 / 7773
页数:13
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