A landscape of synthetic viable interactions in cancer.
OBJECTIVE This study is to identify pediatric brain tumors (PBT) driver genes and key pathways to detect the expression of the driver genes and also to clarify the relationship between patients' prognosis and expression of driver genes. METHODS The gene expression profile of GSE50161 was analyzed to identify the differentially expressed genes (DEGs) between tumor tissue and the normal tissue. Gene ontology, Kyoto Encyclopedia of Genes and Genomes analysis, and protein-protein interaction network analysis were conducted to identify the enrichment functions, pathways, and hub genes. After hub genes were identified, quantitative reverse transcription polymerase chain reaction was used to confirm the differential expression of these hub genes. Survival data of 325 patients' were analyzed to clarify the relationship between prognosis and expression levels of the mutual hub genes. RESULTS Gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis showed that there were 13 common functions and 3 common pathways which were upregulated or downregulated among the 4 groups. Mutual hub genes were somatostatin (SST), glutamate decarboxylase 2 (GAD2), and single copy human parvalbumin gene (PVALB). The expression of SST, GAD2, and PVALB in glioma cells significantly decreased compared with normal glial cells (P < 0.05). In addition, survival analysis showed a favorable progression-free and overall survival in patients with glioma with SST, GAD2, and PVALB high expression (P < 0.05). CONCLUSIONS SST, GAD2, and PVALB significantly decrease in glioma cells compared with normal glial cells. Survival analysis suggests that patients with high-expressed SST, GAD2, and PVALB have a longer overall and progression-free survival. The differential expressed genes identified in this study provide novel targets for diagnosis and treatment.