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Functional Role of miR-138-5p and miR-200b-3p in Testicular Germ Cell Tumors: Molecular Insights into Seminoma and Teratoma Pathogenesis
Functional Role of miR-138-5p and miR-200b-3p in Testicular Germ Cell Tumors: Molecular Insights into Seminoma and Teratoma Pathogenesis
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Functional Role of miR-138-5p and miR-200b-3p in Testicular Germ Cell Tumors: Molecular Insights into Seminoma and Teratoma Pathogenesis
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Functional Role of miR-138-5p and miR-200b-3p in Testicular Germ Cell Tumors: Molecular Insights into Seminoma and Teratoma Pathogenesis
Functional Role of miR-138-5p and miR-200b-3p in Testicular Germ Cell Tumors: Molecular Insights into Seminoma and Teratoma Pathogenesis

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Functional Role of miR-138-5p and miR-200b-3p in Testicular Germ Cell Tumors: Molecular Insights into Seminoma and Teratoma Pathogenesis
Functional Role of miR-138-5p and miR-200b-3p in Testicular Germ Cell Tumors: Molecular Insights into Seminoma and Teratoma Pathogenesis
Journal Article

Functional Role of miR-138-5p and miR-200b-3p in Testicular Germ Cell Tumors: Molecular Insights into Seminoma and Teratoma Pathogenesis

2025
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Overview
This study aims to investigate the molecular mechanisms underlying germ cell tumors (GCTs), focusing specifically on seminomas and teratomas. By analyzing gene expression profiles and miRNA interactions, the goal is to identify key regulatory miRNAs and signaling pathways that differentiate these tumor types and could serve as important regulators for therapy development. Raw data for seminomas and teratomas were extracted from the GEO database, and gene hubs were identified using STRING and Gephi. Signaling pathways and functional annotations were analyzed using miRPathDB, while miRNA–gene interactions were explored via miRWalk. Hub miRNAs were filtered and confirmed using miRDB. This study highlights significant changes in gene expression diversity between tumor and normal gonadal tissues, providing insights into the molecular dynamics of seminomas and teratomas. Distinctions between seminomas and teratomas were identified, shifting the focus toward miRNAs to discover more precise and novel therapeutic approaches. The hub genes of seminomas and teratomas were identified separately. MiRNAs targeting these hub genes were also determined and confirmed. These miRNAs collectively influence essential oncogenic pathways—confirming hsa-miR-138-5p as a regulator of pathways such as Hippo signaling, transcriptional misregulation in cancer, and microRNA cancer signaling in seminomas, and hsa-miR-200b-3p as a regulator of p53 signaling, T cell receptor signaling, and pathways including PI3K/AKT, MAPK/ERK, and Wnt/β-catenin in teratomas—confirming their potential as promising candidates for subtype-specific therapeutic intervention. MiRNAs identified through bioinformatics analyses, and their predicted regulatory roles in key oncogenic pathways, represent potential therapeutic targets or regulators of biological processes. However, further experimental validation is needed to confirm these findings.