Identification of genes and pathways in nasopharyngeal carcinoma by bioinformatics analysis
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Fang Chen1, Congxiang Shen1, Xiaoqi Wang1, Huigang Wang1, Yanhui Liu2, Chaosheng Yu3, Jieyu lv4, Jingjing He5 and Zhong Wen1
1Department of Otorhinolaryngology-Head and Neck Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, China
2Department of Otorhinolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Xinjiang Medical University, Xinjiang, China
3Department of Otorhinolaryngology-Head and Neck Surgery, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, China
4Department of Otorhinolaryngology-Head and Neck Surgery, Jiangmen Central Hospital, Jiangmen, China
5Department of Otorhinolaryngology-Head and Neck Surgery, The First Affiliated Hospital of Xiamen University, Xiamen, China
Zhong Wen, email: [email protected]
Keywords: nasopharyngeal carcinoma, differentially expressed genes, functional enrichment analysis, protein–protein interaction (PPI) network, hub genes
Received: April 13, 2017 Accepted: June 30, 2017 Published: July 22, 2017
Nasopharyngeal carcinoma is a metastatic malignant tumor originating from nasopharyngeal epithelium. Lacking or nonspecific symptoms of patients with early stage nasopharyngeal carcinoma have significantly reduced the accuracy of diagnosing and predicting nasopharyngeal carcinoma development. This study aimed to identify gene signatures of nasopharyngeal carcinoma and uncover potential mechanisms. Two gene expression profiles (GSE12452 and GSE13597) containing 56 nasopharyngeal carcinoma samples and 13 normal control samples were analyzed to identify the differentially expressed genes. In total, 179 up-regulated genes and 238 down-regulated genes were identified. Functional and pathway enrichment analysis showed that up-regulated genes were significantly involved in cell cycle, oocyte meiosis, DNA replication and p53 signaling pathway, while down-regulated genes were enriched in Huntington’s disease,metabolic pathways. Subsequently, the top 10 hub genes, TOP2A (topoisomerase (DNA) II alpha), CDK1 (cyclin-dependent kinase 1), CCNB1 (cyclin B1), PCNA (proliferating cell nuclear antigen), MAD2L1 (mitotic arrest deficient 2 like 1), BUB1 (budding uninhibited by benzimidazoles 1 homolog), CCNB2 (cyclin B2), AURKA (aurora kinase A), CCNA2 (cyclin A2), CDC6 (cell division cycle 6 homolog), were identified from protein-protein interaction network. Furthermore, Module analysis revealed that the ten hub genes except TOP2A were belonged to module 1, indicating the upregulation of these hub genes associated molecular pathways in nasopharyngeal carcinoma might activate nasopharyngeal carcinoma pathogenesis. In conclusion, this study indicated that the identified differentially expressed genes and hub genes enrich our understanding of the molecular mechanisms of nasopharyngeal carcinoma, which could eventually translate into additional biomarkers to facilitate the early diagnosis and therapeutic approaches.
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