Background: Kinesin family member 18A (KIF18A) belongs to a member of the kinesin superfamily and is significantly overexpressed and abnormally functions in a variety of cancers. However, the expression profiling and the role of KIF18A has so far remained unclear in glioma. To investigate the relationship of KIF18A with clinical practice and its role in gliomas, the data from multi public datasets were used and analyzed in present study.Methods: Patients with gliomas were enrolled from CGGA RNA-seq, TCGA-seq, CGGA-microarray, GSE4290 and GSE50161 databases. The expression of KIF18A in glioma and normal tissues was analyzed through Wilcoxon rank sum test, and the relationship between KIF18A and clinicopathological features was evaluated using logistic regression. The effect of KIF18A expression in the survival of glioma patients was explored by Kaplan-Meier and Cox analyses. Gene set enrichment analysis was also conducted to annotate biological function of KIF18A.Results: KIF18A expression was significantly increased in glioma tissues compared with the normal counterparts. High KIF18A expression shortened the overall survival in all grades gliomas and the survival period of patients with WHO grade Ⅲ glioma, but not significantly for grade Ⅱ and grade Ⅳ glioma. Univariate and multivariate analyses demonstrated that evaluated KIF18A expression is closely related to poor prognosis. Increased KIF18A expression was significantly correlated grades, age, IDH wide type and may serve as a biomarker of poor prognosis in gliomas. GSEA showed that the KEGG_DNA_REPLICATION, the KEGG_CELL_CYCLE, the KEGG_MISMATCH_REPAIR and the KEGG_NUCLEOTIDE_EXCISION_REPAIR were differentially enriched in KIF18A high expression phenotype.Conclusions: High expression KIF18A might be potential biomarker for the diagnosis and an independent risk factor for poor prognosis in glioma.