Research Paper Volume 12, Issue 9 pp 7761—7773
MicroRNA-1298-3p inhibits proliferation and invasion of glioma cells by downregulating Nidogen-1
- 1 Department of Ophthalmology, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning, P.R. China
- 2 Department of Neurosurgery, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, P.R. China
received: November 16, 2019 ; accepted: March 29, 2020 ; published: April 30, 2020 ;https://doi.org/10.18632/aging.103087
How to Cite
Copyright © 2020 Xu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.