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Updated: Jan 20, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MicroRNA-181 inhibits glioblastoma cell growth by directly targeting CCL8
Fengyu Zhai1,2, Xinfeng Chen1,3, Qianyi He4
1Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
Abstract:
MicroRNAs (miRNAs/miRs), including miR-181, are closely linked to the development and progression of glioblastoma. However, the function of miR-181 in glioblastoma has not been fully clarified. The aim of the present study was to investigate the role of miR-181 in glioblastoma. miR-181 was revealed to be downregulated in glioblastoma tissues and cell lines, and associated with poor prognosis in patients with glioblastoma. Overexpression of miR-181 inhibited glioblastoma cell proliferation, invasion and migration, arrested glioblastoma cell cycle in the G1 phase and induced glioblastoma cell apoptosis. miR-181 was demonstrated to decrease expression of C-C motif chemokine ligand 8 (CCL8) by directly interacting with its 3'-untranslated region. Overexpression of CCL8 inversely reversed the proliferation, invasion and migration-promoting effects of miR-181 in glioblastoma cells. Furthermore, CCL8 was upregulated in glioblastoma tissues and was negatively correlated with miR-181 expression. These results indicate that miR-181 is a potential molecular biomarker or therapeutic target in the clinical management of glioblastoma.
Insights
MicroRNA-181 (miR-181) is downregulated in glioblastoma, hindering tumor growth and progression. Restoring miR-181 levels shows therapeutic potential for glioblastoma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) play crucial roles in cancer development.
- The specific function of miR-181 in glioblastoma remains unclear.
- Glioblastoma is an aggressive brain tumor with limited treatment options.
Purpose of the Study:
- To investigate the role of miR-181 in glioblastoma.
- To determine the molecular mechanisms underlying miR-181's function.
- To evaluate miR-181 as a potential therapeutic target.
Main Methods:
- Analysis of miR-181 expression in glioblastoma tissues and cell lines.
- Overexpression of miR-181 in glioblastoma cells.
- Assessment of cell proliferation, invasion, migration, cell cycle, and apoptosis.
- Luciferase reporter assays to confirm direct interaction between miR-181 and CCL8.
- Overexpression of C-C motif chemokine ligand 8 (CCL8) to reverse miR-181 effects.
Main Results:
- miR-181 was significantly downregulated in glioblastoma tissues and cell lines.
- Low miR-181 expression correlated with poor patient prognosis.
- miR-181 overexpression suppressed glioblastoma cell proliferation, invasion, and migration.
- miR-181 induced cell cycle arrest at G1 phase and promoted apoptosis.
- miR-181 directly targeted and reduced CCL8 expression.
- CCL8 was upregulated in glioblastoma and its effects were opposite to miR-181.
Conclusions:
- miR-181 acts as a tumor suppressor in glioblastoma.
- The miR-181/CCL8 axis is a key regulator of glioblastoma progression.
- miR-181 is a promising molecular biomarker and therapeutic target for glioblastoma.
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