SYST-23 CDK1 AS AN INDEPENDENT PROGNOSTIC INDICATOR AND POTENTIAL THERAPEUTIC TARGET IN GLIOMA

Glioma is the most common primary malignant tumor in the brain with extremely poor prognosis. Firstly, in order to find the important genes and mechanisms involved in the initiation and progression of glioma, we selected four groups of gene expression profiles from GEO dataset include GSE29796, GSE4290, GSE50161 and GSE7696 for comprehensive data analysis. We identified 360 differentially expressed genes (DEGs), then we screened out core gene which is CDK1 by protein-protein interaction (PPI) network analysis. So as to clarify whether CDK1 is an independent prognostic factor for glioma, we performed expression analysis and prognostic analysis. Meanwhile, in order to verify the expression and survival of CDK1, we used Western blot to detect CDK1 expression of 15 glioma specimens and corresponding adjacent tissues. Moreover, we divided the expression values of CDK1 gene in the CGGA database into high and low groups based on the median for differential expression analysis. Finally, to explore the molecular mechanism of action of CDK1 in gliomas, we conducted gene ontology (GO) enrichment analysis and gene collection enrichment analysis (GSEA),and performed gene co-expression analysis. The results revealed that the expression level of CDK1 in glioma was significantly higher than normal tissues, its high expression was closely associated with poor survival of glioma. And the prognostic analysis showed that CDK1 was an independent prognostic index of glioma. Through the mechanism analysis of GO and GSEA, it is demonstrated that CDK1 plays an important role in the mitosis cell cycle of glioma, and inhibiting the expression of CDK1 can affect the proliferation of glioma cells. Coexpression analysis displayed that the high expression of PCNA, MCM2, MCM3, MCM4, MCM6, PLK1, TTK and MAD2L1 are also correlated to the poor survival and prognosis of glioma. Hence CDK1 is an independent prognostic factor and potential therapeutic target of glioma. Furthermore ,we can affect the proliferation of glioma cells through inhibiting the expression of CDK1.