Bioinformatics analysis reveals disturbance mechanism of MAPK signaling pathway and cell cycle in Glioblastoma multiforme |
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Authors: | Wusheng Li Kai LiLi Zhao Huawei Zou |
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Affiliation: | Department of Oncology, Shengjing Hospital of China Medical University, Shenyang 110023, China |
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Abstract: | Background & objectivesTo analyze the reversal gene pairs and identify featured reversal genes related to mitogen-activated protein kinases (MAPK) signaling pathway and cell cycle in Glioblastoma multiforme (GBM) to reveal its pathogenetic mechanism.MethodsWe downloaded the gene expression profile GSE4290 from the Gene Expression Omnibus database, including 81 gene chips of GBM and 23 gene chips of controls. The t test was used to analyze the DEGs (differentially expressed genes) between 23 normal and 81 GBM samples. Then some perturbing metabolic pathways, including MAPK (mitogen-activated protein kinases) and cell cycle signaling pathway, were extracted from KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway database. Cancer genes were obtained from the database of Cancer Gene Census. The reversal gene pairs between DEGs and cancer genes were further analyzed in MAPK and cell cycle signaling pathway.ResultsA total 8523 DEGs were obtained including 4090 up-regulated and 4433 down-regulated genes. Among them, ras-related protein rab-13(RAB13), neuroblastoma breakpoint family member 10 (NBPF10) and disks large homologue 4 (DLG4) were found to be involved in GBM for the first time. We obtained MAPK and cell cycle signaling pathways from KEGG database. By analyzing perturbing mechanism in these two pathways, we identified several reversal gene pairs, including NRAS (neuroblastoma RAS) and CDK2 (cyclin-dependent kinase 2), CCND1 (cyclin D1) and FGFR (fibroblast growth factor receptor). Further analysis showed that NRAS and CDK2 were positively related with GBM. However, FGFR2 and CCND1 were negatively related with GBM.Interpretation & conclusionsThese findings suggest that newly identified DEGs and featured reversal gene pairs participated in MAPK and cell cycle signaling pathway may provide a new therapeutic line of approach to GBM. |
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Keywords: | BH, Benjamin and Hochberg CAMs, cell adhesion molecules CCND1, cyclin D1 CDK2, cyclin-dependent kinase 2 DEGs, differentially expressed genes DLG4, disks large homologue 4 EGFR, epidermal growth factor receptor FDR, false discovery rate FGFR, fibroblast growth factor receptor GBM, Glioblastoma multiforme KEGG, Kyoto Encyclopedia of Genes and Genomes MAPK, mitogen-activated protein kinases NBPF10, neuroblastoma breakpoint family member 10 NRAS, neuroblastoma RAS PDGFR, platelet-derived growth factor receptor RMA, robust multiarray average RAB13, ras-related protein rab-13 TGF, transforming growth factor VEGF, vascular endothelial growth factor |
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