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Updated: Feb 3, 2026

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
Published on: April 13, 2018
MicroRNA-129-5p inhibits human glioma cell proliferation and induces cell cycle arrest by directly targeting DNMT3A
Xuhui Gu1, Hui Gong1, Lili Shen1
1Department of Neurosurgery, Haimen People's Hospital Haimen 226100, Jiangsu Province, China.
Background:
Glioma is the most common malignant tumor in the adult human brain and has one of the lowest patient survival rates. MicroRNAs (miRNAs) play important roles in the development of cancers, including glioma, and potentially have valuable therapeutic applications in glioma; however, their specific functions and mechanisms of action have yet to be fully defined. Here, we report that miR-129-5p directly targets DNA (cytosine-5)-methyltransferase 3A (DNMT3A) and functions as a tumor-suppressor in glioma.
Method:
We analyzed the expression profiles of miR-129-5p and DNMT3A in glioma-related databases. Quantitative reverse transcription-PCR was applied to detect the level of miR-129-5p in glioma specimens and cell lines. Western blotting was applied to detect the level of DNMT3A. We examined the effect of miR-129-5p on the cell cycle and proliferation of glioma cells using CCK-8 and EDU assays and flow cytometry. TargetScan software predicted DNMT3A to be a target of miR-129-5p, which we confirmed by means of luciferase reporter assays and rescue experiments.
Result:
miR-129-5p was expressed at low levels in glioma and negatively correlated with glioma grade. Over-expression of miR-129-5p in U87and LN229 cells inhibited proliferation and blocked the cell cycle in G1 Phase. DNMT3A is a direct target of miR-129-5p, and miR-129-5p affects glioma cell proliferation by targeting DNMT3A.
Conclusion:
Taken together, our results demonstrate that miR-129-5p plays a significant role in glioma suppression through inhibition of DNMT3A, which may provide a novel therapeutic strategy for treatment of glioma and other DNMT3A-driven cancers.
Insights
MicroRNA-129-5p acts as a tumor suppressor in glioma by targeting DNMT3A. Lower miR-129-5p levels correlate with higher glioma grade, suggesting its therapeutic potential.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Glioma is a prevalent and aggressive brain tumor with poor patient outcomes.
- MicroRNAs (miRNAs) are implicated in cancer development, offering potential therapeutic avenues for glioma.
- The precise roles and mechanisms of miRNAs in glioma remain incompletely understood.
Purpose of the Study:
- To investigate the function of miR-129-5p in glioma.
- To identify the direct molecular targets of miR-129-5p in glioma cells.
- To explore the therapeutic potential of miR-129-5p in glioma treatment.
Main Methods:
- Analysis of miR-129-5p and DNMT3A expression in glioma databases and patient samples.
- Quantitative reverse transcription-PCR and Western blotting to assess expression levels.
- Cellular assays (CCK-8, EDU, flow cytometry) to evaluate proliferation and cell cycle effects.
- Luciferase reporter assays and rescue experiments to confirm direct targeting of DNMT3A by miR-129-5p.
Main Results:
- miR-129-5p expression was significantly reduced in glioma tissues and inversely correlated with tumor grade.
- Overexpression of miR-129-5p inhibited glioma cell proliferation and induced G1 cell cycle arrest.
- DNA (cytosine-5)-methyltransferase 3A (DNMT3A) was validated as a direct target of miR-129-5p.
- miR-129-5p exerts its tumor-suppressive effects by regulating DNMT3A in glioma cells.
Conclusions:
- miR-129-5p functions as a tumor suppressor in glioma by directly inhibiting DNMT3A.
- This miR-129-5p/DNMT3A axis represents a potential novel therapeutic target for glioma.
- The findings suggest a new treatment strategy for glioma and other cancers driven by DNMT3A.
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