Xuan Wang1, Xudong Li1, Yan Zhou1, Xing Huang1, Xiaobing Jiang2. 1. Department of Neurosurgery, Union Hospital of Tongji Medical College Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Jianghan District, Wuhan, 430022, Hubei, China. 2. Department of Neurosurgery, Union Hospital of Tongji Medical College Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, Jianghan District, Wuhan, 430022, Hubei, China. Jiangxiaobing02013@outlook.com.
Abstract
OBJECTIVE: Long 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. METHODS: OIP5-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. RESULTS: OIP5-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. CONCLUSION: OIP5-AS1 inhibition upregulated miR-129-5p to repress resistance to TMZ in GBM cells via downregulating IGF2BP2.
OBJECTIVE: Long 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. METHODS:OIP5-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. RESULTS:OIP5-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. CONCLUSION:OIP5-AS1 inhibition upregulated miR-129-5p to repress resistance to TMZ in GBM cells via downregulating IGF2BP2.
Entities:
Keywords:
Drug resistance; Glioblastoma; Insulin-like growth factor 2 mRNA-binding protein 2; Long non-coding RNA OIP5 antisense RNA 1; MicroRNA-129-5p; Temozolomide
Authors: Jianfeng Gan; Zhixian Chen; Xuan Feng; Zhi Wei; Sai Zhang; Yan Du; Congjian Xu; Hongbo Zhao Journal: Int J Med Sci Date: 2022-01-01 Impact factor: 3.738