FAM111B as a biomarker influences the prognosis and immune microenvironment of low-grade gliomas.

Background: In recent years, FAM111B has been found to be closely related to the occurrence and development of various cancers. However, the role of FAM111B in low-grade glioma (LGG) remains unclear.

Objective: This study aims to investigate the regulatory role of FAM111B in the progression of LGG.

Method: First, this study explored the expression levels of FAM111B in LGG using various databases. Second, Wilcoxon and Kruskal-Wallis tests were employed to assess the association between FAM111B expression and clinical characteristics. Survival analysis and multivariate Cox regression evaluated the prognostic value of FAM111B expression levels in LGG. Additionally, GSEA was performed to explore pathways associated with FAM111B expression, while Pearson correlation analysis revealed relationships between FAM111B expression and tumor-associated macrophages as well as immune checkpoints.

Results: The findings of this study demonstrate that high expression of FAM111B is significantly associated with molecular characteristics of LGG. FAM111B serves as an independent prognostic factor, and the high expression of FAM111B significantly shortens survival of LGG patients. The methylation site cg14859464 was found to negatively regulate FAM111B expression. FAM111B primarily activates pathways related to Cell cycle regulation, DNA replication, and Mismatch repair. Additionally, FAM111B expression showed positive correlations with macrophage marker CD163 and immune checkpoint molecule CD276.

Conclusion: This study conducted an in-depth investigation into the biological functions of FAM111B in LGG. We identified FAM111B as an independent prognostic factor associated with unfavorable clinical outcomes in LGG. The findings provide novel insights and actionable targets for the precise diagnosis and effective management of LGG.