Document Type : Research Articles
Authors
1
Department of Cell and Molecular Biology & Microbiology, Faculty of Biological Science and Technology, University of Isfahan, HezarJarib Street, Isfahan 81746-73441, Iran
2
1Department of Cell and Molecular Biology & Microbiology, Faculty of Biological Science and Technology, University of Isfahan, HezarJarib Street, Isfahan 81746-73441, Iran
3
1Department of Cell and Molecular Biology & Microbiology, Faculty of Biological Science and Technology, University of Isfahan, HezarJarib Street, Isfahan 81746-73441, Iran
4
2Department of Genetics and Molecular Biology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran 3Reproductive Sciences and Sexual Health Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
10.22067/jcmr.2026.97475.1127
Abstract
Background Medulloblastoma (MB) is the most common malignant pediatric brain tumor, characterized by molecular heterogeneity and aggressiveness. The Musashi-1 (MSI1) pathway has recently garnered significant interest as a central mediator of medulloblastoma tumorigenesis and tumor growth. The RNA-binding protein (MSI1) has been identified as a key regulator of MB tumorigenesis, promoting cancer stem cell phenotypes and treatment resistance. MSI1 research in medulloblastoma also includes its potential as a prognostic and diagnostic biomarker. Methods In the current study, the role of MSI1 in medulloblastoma was highlighted using differential expression and weighted gene co-expressio network analysis. In this study, the role of MSI1 in Medulloblastoma was explored through bioinformatics analysis of RNA-Seq data of 93 MB samples (GEO datasets: GSE143940, GSE158413, GSE189919) and 266 normal cerebellum samples (GTEx). DESeq2 package was used for differential expression analysis, and WGCNA was employed for the discovery of MSI1-associated co-expression networks. Results A total of 11,055 significantly differentially expressed genes were identified in Medulloblastoma, comprising 5,925 upregulated and 5,130 downregulated genes. WGCNA positioned MSI1 in the Medulloblastoma-specific, non-preserved darkgrey module with hub genes ANO2 (Log2FC: 4.80, p = 0) and CACNA1F (Log2FC: 2.18, p = 9.59E-65), implicating them in MSI1-driven oncogenic mechanisms. MSI2, on the other hand, was positioned in a preserved module, suggesting a more general function. Conclusion These findings highlight MSI1's specificity to Medulloblastoma and its potential as a biomarker and therapeutic target. Upregulation of ANO2 and CACNA1F, as well as MSI1's role in tumor aggressiveness, underscores the need for additional functional exploration to validate their therapeutic relevance. This research helps develop customized treatments to improve outcomes in MB patients.
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