MAD2L2 as a novel prognostic biomarker and its correlation with immune infiltrates in glioma

Abstract

Background: The most common type of central nervous system tumor is glioma, the identification of Glioma biomarkers is essential. MAD2L2, which is abbreviated as MAD2-Like2, collaborates with a number of proteins to carry out numerous essential cellular functions. Uncertain is the role of MAD2L2 in glioma. The role of MAD2L2 expression is examined for the first time in relation to gliomas occurrence and development in this study Methods: A bioinformatics and clinicopathological analysis, immune infiltration analysis, and enrichment analysis were conducted based on TCGA and additional gene expression analysis. Using ssGSEA and TIMER, the immune response to MAD2L2 expression in glioma was analyzed statistically. This study also analyzed the effect of MAD2L2 overexpression on major chemotherapeutic medicines and the methylation status of glioma patients. CGGA, HPA data analysis, and K-M survival were also utilized to validate the results. Results: MAD2L2 was a crucial independent prognostic factor for glioma patients. Correlations were found between MAD2L2 expression and age, IDH status, WHO grades and 1p/19q codeletion. MAD2L2 is intimately connected to the DNA replication, transcription, cell cycle, immune system, and signal transduction pathways, as determined by the GSEA. In glioma, The majority of MAD2L2 DNA methylation sites were hypomethylated, and the degree of methylation was associated with patient outcomes. Chemotherapy would benefit MAD2L2 overexpression patients. according to these results. The expression of MAD2L2 was associated with partial immune cell infiltration and co-expressed with immune-related genes and immune checkpoints. Conclusion: Glioma is characterized by higher MAD2L2 expression, and high MAD2L2 expression is linked with a poor prognosis. MAD2L2 might participate in tumor development by regulating tumor-infiltrating cells inside the TME. MAD2L2 could possibly be an immunotherapeutic target.