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Updated: Jul 18, 2025
08:40
Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
Published on: April 6, 2012
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MicroRNAs miR-16 and miR-519 control meningioma cell proliferation via overlapping transcriptomic programs shared
Sébastien Hergalant1, Jean-Matthieu Casse1, Abderrahim Oussalah1,2,3
1INSERM, U1256, NGERE - Nutrition, Genetics, and Environmental Risk Exposure, Faculty of Medicine of Nancy, University of Lorraine, Vandoeuvre-lès-Nancy, France.
Frontiers in Oncology
|August 21, 2023
Summary
Decreased miR-16 and miR-519 levels correlate with human meningioma development. Restoring these microRNAs inhibits tumor cell growth, potentially via HuR inhibition.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Genomics
Background:
- Meningiomas are common primary central nervous system tumors, with most being benign but a subset becoming malignant.
- MicroRNAs (miRs) play crucial roles in cellular processes, including tumorigenesis.
Purpose of the Study:
- To investigate the role of miR-16 and miR-519 in human meningioma development and cell growth.
- To elucidate the molecular mechanisms underlying the function of these miRs in meningioma.
Main Methods:
- Quantification of miR-16 and miR-519 expression in human meningioma tissues and cell lines.
- Cell growth assays and transcriptome analysis following miR mimic transfection.
- Integrative bioinformatics analysis of transcriptomic data.
Main Results:
- Lower levels of miR-16 and miR-519 were observed in tumoral tissues compared to healthy controls.
- Overexpression of miR-16 or miR-519 significantly reduced meningioma cell growth.
- Downregulated genes in response to miR-16/miR-519 included ELAVL1/HuR, impacting cell cycle and brain development pathways.
Conclusions:
- miR-16 and miR-519 exhibit tumor suppressor functions in human meningiomas.
- Their tumor-suppressive effects are, at least partially, mediated through the inhibition of HuR.
- These findings highlight the potential of miR-16 and miR-519 as therapeutic targets for meningioma.
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