Long non-coding RNA OIP5-AS1 inhibition upregulates microRNA-129-5p to repress resistance to temozolomide in glioblastoma cells via downregulating IGF2BP2

被引:22
|
作者
Wang, Xuan [1 ]
Li, Xudong [1 ]
Zhou, Yan [1 ]
Huang, Xing [1 ]
Jiang, Xiaobing [1 ]
机构
[1] Huazhong Univ Sci & Technol, Dept Neurosurg, Union Hosp, Tongji Med Coll, 1277 Jiefang Ave, Wuhan 430022, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
Glioblastoma; Long non-coding RNA OIP5 antisense RNA 1; MicroRNA-129-5p; Insulin-like growth factor 2 mRNA-binding protein 2; Temozolomide; Drug resistance; PROLIFERATION; GLIOMA; MECHANISMS; MIGRATION;
D O I
10.1007/s10565-021-09614-z
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
ObjectiveLong non-coding RNAs (lncRNAs) and miRNAs (miRNAs) participate in tumors, while the effects of lncRNA OIP5 antisense RNA 1 (OIP5-AS1) and miR-129-5p on glioblastoma (GBM) remain to be further studied. We aim to explore the role of OIP5-AS1/miR-129-5p/insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) axis in GBM progression.MethodsOIP5-AS1, miR-129-5p and IGF2BP2 expression in tissues was determined. Temozolomide (TMZ)-resistant GBM cells were established and transfected with relative plasmid to alter OIP5-AS1, IGF2BP2 or miR-129-5p expression. Then, the viability, proliferation, apoptosis and in vivo tumor growth were assessed. The subcellular localization of OIP5-AS1 was determined, and the binding relationships between OIP5-AS1 and miR-129-5p, and between miR-129-5p and IGF2BP2 were confirmed.ResultsOIP5-AS1 and IGF2BP2 were upregulated whereas miR-129-5p was downregulated in GBM. OIP5-AS1 silencing or miR-129-5p overexpression inhibited GBM cell chemoresistance to TMZ and proliferation, and promoted cell apoptosis. MiR-129-5p downregulation or IGF2BP2 upregulation reversed the role of OIP5-AS1 silencing on GBM cells. OIP5-AS1 sponged miR-129-5p and miR-129-5p targeted IGF2BP2.ConclusionOIP5-AS1 inhibition upregulated miR-129-5p to repress resistance to TMZ in GBM cells via downregulating IGF2BP2.
引用
收藏
页码:963 / 977
页数:15
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