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Updated: May 4, 2026

Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
MicroRNA-155 promotes glioma cell proliferation via the regulation of MXI1
Jianwen Zhou1, Wei Wang2, Zhenhua Gao3
1State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China ; Key Laboratory of Gene Engineering of the Ministry of Education, School of Life Sciences, Sun Yat-sen University, Guangzhou, China ; Department of Pathology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Abstract:
Gliomas are the most common and aggressive primary tumors in the central nervous system. Recently, Max interactor-1 (MXI1), an antagonist of c-Myc that is involved in brain tumor progression, has been reported to be deregulated in a variety of tumors including glioma. However, the mechanism of MXI1 deregulation in gliomas remains unclear. In this study, we show that the relative expression level of MXI1 is markedly down-regulated in glioma cell lines. Using integrated bioinformatic analysis and experimental confirmation, we identified several miRNAs by screening a panel of predicted miRNAs that may regulate the MXI1 3'UTR. The strongest inhibitory miRNA, miR-155, can attenuate the activity of a luciferase reporter gene that is fused with the MXI1 3'UTR and decrease the expression levels of MXI1 mRNA and protein in U87 glioma cells. The potential role of miR-155 in promoting glioma cell proliferation by targeting MXI1 was confirmed in various glioma cell lines by rescue experiments using MTT assays, EdU incorporation assay, and cell counting experiments. In addition, we determined that the level of MXI1 mRNA was inversely correlated with the expression of miR-155 in 18 sets of glioblastoma multiforme specimens. These findings reveal for the first time that the targeting of MXI1 by miR-155 may result in a reduction in MXI1 expression and promote glioma cell proliferation; this result suggests a novel function of miR-155 in targeting MXI1 in glioma-genesis.
Insights
MicroRNA-155 (miR-155) targets Max interactor-1 (MXI1) in glioma, reducing its expression and promoting tumor cell proliferation. This study reveals a novel mechanism in glioma-genesis involving miR-155 and MXI1.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Research
Background:
- Gliomas are aggressive primary central nervous system tumors.
- Max interactor-1 (MXI1), a c-Myc antagonist, is deregulated in various tumors, including glioma.
- The precise mechanism of MXI1 deregulation in gliomas is not fully understood.
Purpose of the Study:
- To elucidate the mechanism of MXI1 deregulation in glioma.
- To identify microRNAs (miRNAs) regulating MXI1 expression in glioma cells.
- To investigate the role of miR-155 in glioma progression by targeting MXI1.
Main Methods:
- Bioinformatic analysis and experimental validation to identify regulatory miRNAs.
- Luciferase reporter assays to confirm direct targeting of MXI1 3'UTR by miR-155.
- Cell proliferation assays (MTT, EdU, cell counting) and rescue experiments in glioma cell lines.
- Correlation analysis of miR-155 and MXI1 mRNA levels in glioblastoma specimens.
Main Results:
- MXI1 expression is significantly down-regulated in glioma cell lines.
- miR-155 was identified as a potent inhibitor of MXI1, reducing its mRNA and protein levels in U87 cells.
- miR-155 promotes glioma cell proliferation by targeting MXI1, confirmed through rescue experiments.
- Inverse correlation observed between MXI1 mRNA and miR-155 expression in glioblastoma samples.
Conclusions:
- miR-155 directly targets MXI1, leading to decreased MXI1 expression and enhanced glioma cell proliferation.
- This study uncovers a novel role for miR-155 in glioma-genesis through the suppression of MXI1.
- Targeting the miR-155/MXI1 axis presents a potential therapeutic strategy for gliomas.
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