Comprehensive analysis of FAM111B as an emerging prospective biomarker in glioma


Abstract

Background : The FAM111B has a significant part to perform in the pathogenesis of certain tumors, but its relationship with glioblastoma remains unclear. This research aims to probe the expression of FAM111B in glioblastoma and to analyze the relationship between FAM111B expression and the prognosis of patients. Methods : Using the TCGA and the GTEx, the gene levels of FAM111B in glioma tissue and control tissue were investigated. Additionally, the expression of FAM111B in glioma was further verified through IHC of the Human Protein Atlas. The associations from FAM111B to glioma prognosis were interrogated by using Kaplan-Meier analysis and COX regression analysis. With help from nomograms, we anticipate the survival of glioma patients. The effect of FAM111B on the proliferation of glioma cells was investigated in the LN229 cell line. The gene associated with FAM111B was instrumented with functional enrichment analysis by utilizing GO and KEGG functional analysis. The correlation between FAM111B and m6A modification in glioma was analyzed. Immune infiltration analysis was carried out basing on single-sample GSEA. Results : In TCGA, the presence of FAM111B is notable in many types of cancer. Comparative analysis reveals a meaningful upregulation of FAM111B in glioma relative to normal counterparts. The upregulation of FAM111B is associated with poorer clinical pathological features of glioma. By interfering with the expression of FAM111B, the proliferation ability of LN229 cells significantly decreased. It has been determined that the enrichment of FAM111B-related genes is principally concerned with biological processes. FAM111B is affiliated with most m6A-related genes. The infiltration of immune cells in glioma is linked to FAM111B, which is also related to the expression of Th2. Conclusion : Elevated expression of FAM111B is accompanied by an adverse prognosis in patients with glioma, and it has been posited that its function may be implicated in m6A methylation. FAM111B inhibits the proliferative capacity of glioma cells. FAM111B is engaged in the process of immune infiltration of glioma.
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