Abstract | OBJECTIVE: 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.
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Authors | Xuan Wang, Xudong Li, Yan Zhou, Xing Huang, Xiaobing Jiang |
Journal | Cell biology and toxicology
(Cell Biol Toxicol)
Vol. 38
Issue 6
Pg. 963-977
(12 2022)
ISSN: 1573-6822 [Electronic] Switzerland |
PMID | 34132932
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | © 2021. The Author(s), under exclusive licence to Springer Nature B.V. |
Chemical References |
- RNA, Long Noncoding
- MicroRNAs
- Temozolomide
- IGF2BP2 protein, human
- RNA-Binding Proteins
- Mirn129 microRNA, human
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Topics |
- Humans
- RNA, Long Noncoding
(genetics, metabolism)
- MicroRNAs
(genetics, metabolism)
- Temozolomide
(pharmacology)
- Glioblastoma
(drug therapy, genetics)
- Gene Expression Regulation, Neoplastic
(genetics)
- Cell Line, Tumor
- Cell Proliferation
(genetics)
- RNA-Binding Proteins
(genetics, metabolism)
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