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Expression characteristics and prognostic value of CENPM, and its mechanisms in regulating malignant phenotypes in glioma
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Abstract:
[Abstract] Objective: To investigate the expression characteristics and clinical prognostic value of centromere protein M (CENPM) in glioma, and its regulatory mechanisms on malignant biological behaviors, providing potential targets for precision therapy in glioma. Methods: Based on the Chinese Glioma Genome Atlas (CGGA) and the Cancer Genome Atlas (TCGA) database, the expression of CENPM in glioma and its correlation with patients' clinicopathological features and prognosis were analyzed. Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, and single-cell transcriptome analysis were performed to explore the biological functions and mechanisms of CENPM. WB was used to detect CENPM expressions in glioma cell lines (LN-18, LN-229, U-138MG, U-251MG) and a normal glial cell line (HEB). After constructing CENPM knockdown cell lines, the alterations in malignant phenotypes were assessed using CCK-8, colony formation, Transwell, and wound healing assays. Results: CENPM was significantly upregulated in WHO high-grade gliomas (P < 0.05) and positively correlated with tumor malignancy. Patients in the high-expression group had significantly shorter overall survival than those in the low-expression group (P < 0.01), and Cox regression confirmed CENPM as an independent risk factor for glioma prognosis (P < 0.05). Functional enrichment analysis showed that CENPM-related genes were primarily enriched in cell cycle regulation, the PI3K-Akt pathway, and immune-related processes. Single-cell analysis indicated that CENPM was primarily highly expressed in CD8+ T cells and regulated cell communication through the PTN-PTPRZ1/NCL ligand-receptor pair. In vitro experiments confirmed that CENPM expression was higher in glioma cell lines than in normal glial cells (LN-18: P < 0.01, LN-229: P < 0.05); knockdown of CENPM significantly inhibited migration (P < 0.05) but enhanced colony formation, suggesting its dual regulatory role in tumor progression. Conclusion: As an independent prognostic risk factor for glioma, CENPM drives tumor progression by regulating the cell cycle, PTN pathway, and immune microenvironment. Its differential regulatory mechanism (inhibiting migration, promoting proliferation) has potential clinical translational value and can serve as a candidate marker for molecular typing and targeted therapy.
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