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Updated: May 23, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MiR-128 inhibits tumor growth and angiogenesis by targeting p70S6K1
Zhu-mei Shi1, Jing Wang, Zhiping Yan
1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Abstract:
MicroRNAs are a class of small noncoding RNAs that function as critical gene regulators through targeting mRNAs for translational repression or degradation. In this study, we showed that miR-128 expression levels were decreased in glioma, and identified p70S6K1 as a novel direct target of miR-128. Overexpression of miR-128 suppressed p70S6K1 and its downstream signaling molecules such as HIF-1 and VEGF expression, and attenuated cell proliferation, tumor growth and angiogenesis. Forced expression of p70S6K1 can partly rescue the inhibitory effect of miR-128 in the cells. Taken together, these findings will shed light to the role and mechanism of miR-128 in regulating glioma tumor angiogenesis via miR-128/p70S6K1 axis, and miR-128 may serve as a potential therapeutic target in glioma in the future.
Insights
MicroRNAs (miRNAs) regulate genes. This study found decreased miR-128 in glioma, targeting p70S6K1 to inhibit tumor growth and angiogenesis, suggesting miR-128 as a potential therapeutic target.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- MicroRNAs (miRNAs) are key regulators of gene expression, impacting various cellular processes.
- Dysregulation of miRNAs is implicated in the development and progression of various cancers, including glioma.
- Understanding miRNA function is crucial for developing novel cancer therapies.
Purpose of the Study:
- To investigate the role of miR-128 in glioma.
- To identify direct targets of miR-128 in glioma cells.
- To elucidate the mechanism by which miR-128 affects glioma progression, focusing on tumor growth and angiogenesis.
Main Methods:
- Quantitative real-time PCR to measure miR-128 expression levels in glioma tissues.
- Western blotting and luciferase reporter assays to validate p70S6K1 as a direct target of miR-128.
- Cell proliferation assays, in vivo tumor growth models, and assessment of angiogenesis markers (HIF-1, VEGF) following miR-128 or p70S6K1 manipulation.
Main Results:
- miR-128 expression was significantly decreased in glioma tissues compared to normal brain tissues.
- p70S6K1 was identified as a direct target of miR-128, with miR-128 overexpression leading to reduced p70S6K1 levels.
- Overexpression of miR-128 suppressed glioma cell proliferation, tumor growth, and angiogenesis by inhibiting p70S6K1 and its downstream signaling pathways (HIF-1, VEGF).
- Forced expression of p70S6K1 partially rescued the inhibitory effects of miR-128.
Conclusions:
- The miR-128/p70S6K1 axis plays a critical role in regulating glioma tumor growth and angiogenesis.
- miR-128 functions as a tumor suppressor in glioma by targeting p70S6K1.
- miR-128 represents a promising therapeutic target for glioma treatment.
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