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Updated: Aug 23, 2025
Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
In silico characterization of competing endogenous RNA network in glioblastoma multiforme with a systems biology
Soudeh Ghafouri-Fard1, Arash Safarzadeh1, Bashdar Mahmud Hussen2,3
1Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
Glioblastoma multiforme (GBM) is the most frequent malignant type of primary brain cancers and is a malignancy with poor prognosis. Thus, it is necessary to find novel therapeutic modalities based on molecular events occur at different stages of tumor progression. We used expression profiles of GBM tissues that contained long non-coding RNA (lncRNA), microRNA (miRNA) and mRNA signatures to make putative ceRNA networks. Our strategy led to identification of 1080 DEmRNAs, including 777 downregulated DEmRNAs (such as GJB6 and SLC12A5) and 303 upregulated DEmRNAs (such as TOP2A and RRM2), 19 DElncRNAs, including 16 downregulated DElncRNAs (such as MIR7-3HG and MIR124-2HG) and 3 upregulated DElncRNAs (such as CRNDE and XIST) and 49 DEmiRNAs, including 10 downregulated DEmiRNAs (such as hsa-miR-10b-5p and hsa-miR-1290) and 39 upregulated DEmiRNAs (such as hsa-miR-219a-2-3p and hsa-miR-338-5p). We also identified DGCR5, MIAT, hsa-miR-129-5p, XIST, hsa-miR-128-3p, PART1, hsa-miR-10b-5p, LY86-AS1, CRNDE, and DLX6-AS1 as 10 hub genes in the ceRNA network. The current study provides novel insight into molecular events during GBM pathogenesis. The identified molecules can be used as therapeutic targets for GBM.
Insights
Glioblastoma multiforme (GBM) is a deadly brain cancer. This study identifies key molecules and networks involved in GBM progression, offering potential new therapeutic targets for this challenging disease.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor, characterized by a poor prognosis.
- Novel therapeutic strategies are urgently needed, necessitating a deeper understanding of the molecular mechanisms driving GBM progression.
Purpose of the Study:
- To construct competing endogenous RNA (ceRNA) networks using expression profiles of GBM tissues.
- To identify differentially expressed genes (DEGs) including long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs).
- To pinpoint potential therapeutic targets for GBM based on molecular events during tumor progression.
Main Methods:
- Utilized expression profiles of GBM tissues encompassing lncRNA, miRNA, and mRNA signatures.
- Constructed putative ceRNA networks to analyze molecular interactions.
- Identified differentially expressed molecules and hub genes within the ceRNA network.
Main Results:
- Identified 1080 differentially expressed mRNAs (DEmRNAs), 19 differentially expressed lncRNAs (DElncRNAs), and 49 differentially expressed miRNAs (DEmiRNAs).
- Highlighted 10 hub genes in the ceRNA network, including DGCR5, MIAT, hsa-miR-129-5p, XIST, hsa-miR-128-3p, PART1, hsa-miR-10b-5p, LY86-AS1, CRNDE, and DLX6-AS1.
- Revealed significant molecular alterations underlying GBM pathogenesis.
Conclusions:
- The study provides novel insights into the molecular events involved in GBM pathogenesis.
- The identified molecules and hub genes represent promising therapeutic targets for GBM treatment.
- Further investigation of these molecular players could lead to improved therapeutic modalities for GBM.
