Identification of the Interaction Network of Hub Genes for Melanoma Treated with Vemurafenib Based on Microarray Data

细胞周期 生物 E2F型 微阵列分析技术 支票1 细胞周期检查点 转录组 细胞生物学 基因 小桶 遗传学 基因表达
作者
Liangliang Quan,Yang Wang,Jiulong Liang,Jie Shi,Yu Zhang,Kai Tao
出处
期刊:Tumori Journal [SAGE]
卷期号:101 (4): 368-374 被引量:5
标识
DOI:10.5301/tj.5000316
摘要

The objective of this study was to identify possible biomarkers and to explore the mechanisms of suppression of vemurafenib on melanoma progression.GSE42872 affymetrix microarray data were downloaded from the Gene Expression Omnibus database for further analysis. Differentially expressed genes (DEGs) between vehicle-treated samples and vemurafenib-treated samples were identified. Gene ontology and pathway enrichment analysis of DEGs were performed, followed by protein-protein interaction (PPI) network construction. Furthermore, the functional modules of the PPI network were screened using BioNet analysis tool. Finally, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis was performed for DEGs in the module.In total, 794 upregulated transcripts corresponding to 214 genes and 977 downregulated transcripts corresponding to 325 genes were screened. The downregulated DEGs were significantly enriched in pathways such as cell cycle, DNA replication, and p53 signaling pathway. Upregulated DEGs were significantly enriched in phosphatidylinositol signaling system and inositol phosphate metabolism. Significantly enriched functions of downregulated DEGs were mitotic cell cycle, nuclear division, DNA metabolic process, cell cycle, and mitosis. Upregulated DEGs were mainly enriched in single multicellular organism process and multicellular organismal process. Moreover, cell division cycle 6, checkpoint kinase 1 (CHEK1), E2F transcription factor 1 (E2F1), epidermal growth factor receptor (EGFR), and phosphoinositide-3-kinase, regulatory subunit 1-α (PIK3R1) of the module were remarkably enriched in pathways such as cell cycle, apoptosis, focal adhesion, and DNA replication.Cell division cycle 6, CHEK1, E2F1, EGFR, and PIK3R1 of the module and their relative pathways, cell cycle, and focal adhesion might play important roles of suppression of vemurafenib on melanoma progression.
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