Comprehensive Bioinformatics and Functional Analysis Identified MCM5 Facilitates Glioblastoma Progression Through Cell Cycle Regulation.

Minichromosome maintenance protein 5 (MCM5) has emerged as a prominent oncogenic across multiple malignancies. However, its role in glioblastoma (GBM) remains unclear. This study investigates the mechanistic role of MCM5 in GBM pathogenesis. We performed pan-cancer analysis of MCM5 by public datasets (TCGA, GTEx), with particular focus on its expression in GBM, and functional validation by siRNA-mediated knockdown in GBM cell lines (LN18, U87). GO enrichment analysis of MCM5 and its related functional genes was performed using the Metascape database to identify MCM5-related pathways. We subsequently used a variety of experimental methods to thoroughly examine the effect of MCM5 dysfunction on cellular functions, including a subcutaneous hypodermic tumour transplantation model in nude mice, flow cytometry, Transwell assays and wound healing assays. MCM5 exhibited significant overexpression in GBM tissues compared to normal controls. Furthermore, MCM5 expression demonstrated positive correlations with Th2 cells, aCD, and other immune cells. Gene enrichment analysis suggested that MCM5 plays a role in cancer development by regulating deoxyribonucleic acid (DNA) replication. In vitro and in vivo experiments showed that MCM5 enhances GBM cell proliferation, migratory capacity, and cell cycle progression. By bioinformatics analysis and cell experiments, MCM5 is found to promote the progression of GBM by accelerating cell cycle. These findings will provide new clues for the mechanism exploration and prognostic prediction of GBM.