CD93 is Associated with Glioma-related Malignant Processes and Immunosuppressive Cell Infiltration as an Inspiring Biomarker of Survivance

Previous reports have confirmed the significance of CD93 in the progression of multiple tumors; however, there are few studies examining its immune properties for gliomas. Here, we methodically investigated the pathophysiological characteristics and clinical manifestations of gliomas. Six hundred ninety-nine glioma patients in TCGA along with 325 glioma patients in CGGA were correspondingly collected for training and validating. We analyzed and visualized total statistics using RStudio. One-way ANOVA and Student’s t-test were used to assess groups’ differences. All differences were considered statistically significant at the level of P < 0.05. CD93 markedly upregulated among HGG, MGMT promoter unmethylated subforms, IDH wild forms, 1p19q non-codeletion subforms, and mesenchyme type gliomas. ROC analysis illustrated the favorable applicability of CD93 in estimating mesenchyme subform. Kaplan–Meier curves together with multivariable Cox analyses upon survivance identified high-expression CD93 as a distinct prognostic variable for glioma patients. GO analysis of CD93 documented its predominant part in glioma-related immunobiological processes and inflammation responses. We examined the associations of CD93 with immune-related meta-genes, and CD93 positively correlated with HCK, LCK, MHC I, MHC II, STAT1 and IFN, while adverse with IgG. Association analyses between CD93 and gliomas-infiltrating immunocytes indicated that the infiltrating degrees of most immunocytes exhibited positive correlations with CD93, particularly these immunosuppressive subsets such as TAM, Treg, and MDSCs. CD93 is markedly associated with adverse pathology types, unfavorable survival, and immunosuppressive immunocytes infiltration among gliomas, thus identifying CD93 as a practicable marker and a promising target for glioma-based precise diagnosis and therapeutic strategies. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12031-022-02060-4.