Furthermore, parthenolide may function in targeted chemotherapy via the NF-κB/COX2 pathway. It is known that COX2 can regulate cancer stem-like cells of NPC cells and promote their characteristics. As a downstream gene involved in the NF-κB pathway, PTGS2 is also referred to as cyclooxygenase-2 (COX-2). PTGS2, FN1, CXCL9 and CXCL10 were significantly up-regulated genes involved in the TF-DEG regulatory network, and they may function in NPC through ZIC2 or OVOL1 (e.g., ZIC2→PTGS2 and OVOL1→CXCL10).Įnrichment analysis indicated that PTGS2 was involved in the regulation of biological process and small cell lung cancer. There were many functions enriched for the DEGs, such as extracellular matrix organization and extracellular structure organization. In this study, a total of 487 genes were selected as DEGs between NPC samples and normal nasopharyngeal tissue samples, including 122 up-regulated and 365 down-regulated genes. Metabolism of xenobiotics by cytochrome P450

Negative regulation of ryanodine-sensitive calcium-release channel activity Regulation of ryanodine-sensitive calcium-release channel activity Positive regulation of ryanodine-sensitive calcium-release channel activity Regulation of release of sequestered calcium ion into cytosol by sarcoplasmic reticulum In addition, a TF-DEG regulatory network was constructed to investigate the regulatory relationships between TFs and DEGs. The potential functions of the DEGs were predicted by functional and pathway enrichment analyses. 3 Using the same data that was used by Sengupta et al., 3 we not only screened the DEGs but also performed a comprehensive bioinformatic analysis to identify key genes associated with NPC. analyzed the expression of all latent EBV genes between NPC samples and normal nasopharyngeal epithelium samples, and obtained a panel of differentially expressed genes (DEGs). 14, 15 Although these studies have been performed to investigate NPC, the mechanisms of NPC still remain unclear. 13 By down-regulating the expression of Secreted Protein, Acidic and Rich in Cysteine (SPARC), TF sex determining region Y-box 5 (SOX-5) functions in the progression of NPC and may be used as a predictor for poor NPC prognosis. 12 The TF Forkhead Box M1 (FOXM1) is involved in tumor development, and the adenovirus vector AdFOXM1shRNA, which expresses FOXM1-specific short hairpin RNA, may be used as a therapeutic intervention for the treatment of patients with NPC. 10, 11 The transcription factor (TF) adaptor-related protein complex 1 (AP-1) activated by the EBV-encoded Nuclear Antigen 1 (EBNA1) can target hypoxia-inducible factor-1α, interleukin 8 and Vascular Endothelial Growth Factor (VEGF), which promotes microtubule formation in NPC cells. 9 Previous studies show that the potential tumor suppressor gene A disintegrin-like and metalloprotease domain with thrombospondin type 1 motifs 9 (ADAMTS9) is closely related to lymph node metastases, and it can inhibit tumor growth by suppressing angiogenesis in NPC. 6, 7, 8 Disabled 2 (DAB2) is frequently down-regulated by promoter hypermethylation and may be a potential tumor suppressor in NPC. There are several genes (such as C-myc, AKT1, p53, MDM2, LMP1 and PTEN) implicated in the pathogenesis of NPC because they are often amplified or altered in patients with this disease. Many studies investigating the mechanisms of NPC have been published. 5 Therefore, it is of great importance to study the mechanisms of NPC. 4 Most cases of NPC are correlated with Epstein–Barr Virus (EBV) infection, which is a B-lymphotropic herpesvirus possessing growth-transforming properties. 2, 3 NPC can be induced by multiple factors including heredity, viral factors and environmental influences. 1 NPC is extremely common in Southeast Asia and southern China, with more than 50,000 new cases each year. As the most common cancer originating from the nasopharynx, nasopharyngeal carcinoma (NPC) caused approximately 86,700 new cases and 50,800 deaths globally in 2012.

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