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LncRNA MYCNOS promotes glioblastoma cell proliferation by regulating miR-216b/FOXM1 axis

LncRNA MYCNOS promotes glioblastoma cell proliferation by regulating miR-216b/FOXM1 axis

Authors :
Yong Wang
Zhi Li
Ping Zhao
Youliang Wang
Qi Gu
Ting Li
Source :
Metabolic Brain Disease. 36:1185-1189
Publication Year :
2021
Publisher :
Springer Science and Business Media LLC, 2021.

Abstract

MYCNOS is an oncogenic lncRNA in liver cancer, but its role in glioblastoma (GBM) is unknown. We predicted that MYCNOS might interact with miR-216b, which targets FOXM1 to perform tumor suppressive roles. This study was performed to analyze the role of MYCNOS in GBM and explore its potential interactions with miR-216b and FOXM1. MYCNOS expression in paired GBM and non-tumor tissues from 62 GBM patients was analyzed by RT-qPCR. The interaction between MYCNOS and miR-216b was predicted by IntaRNA 2.0 and confirmed by dual luciferase activity assay. Overexpression of MYCNOS, miR-216b, and FOXM1 was achieved in GBM cells, followed by performing RT-qPCR and Western blot to explore the relationship among them. CCK-8 assay was performed to explore the role of MYCNOS, miR-216b, and FOXM1 in regulating GBM cell proliferation. MYCNOS was upregulated in GBM tissues compared to the paired non-tumor tissues. MYCNOS is predicted to interact with miR-216b, but overexpression of MYCNOS and miR-216b failed to affect each other's expression significantly. Dual luciferase activity assay showed that MYCNOS and miR-216b could directly interact with each other. MYCNOS overexpression increased the expression of FOXM1, which is a direct target of miR-216b. Cell proliferation assay showed that MYCNOS and FOXM1 overexpression resulted in an increased proliferation rate of GBM cells, while miR-216b overexpression suppressed cell proliferation. Moreover, MYCNOS overexpression suppressed the role of miR-216b. MYCNOS may regulate FOXM1 expression of by serving as an endogenous sponge of miR-216b axis to promote the proliferation of GBM cells.

Details

ISSN :
15737365 and 08857490
Volume :
36
Database :
OpenAIRE
Journal :
Metabolic Brain Disease
Accession number :
edsair.doi.dedup.....c881900862e5e563fd55e7d0990e69e1
Full Text :
https://doi.org/10.1007/s11011-021-00729-0