![]() ![]() 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. Cytoscape transcription factor pro#(To download the TRANSFAC PRO version, the user will need to have a valid subscription to TRANSFAC Professional).* Cytoscape transcription factor full version#*A full version of the plugin including TRANSFAC Professional motifs is provided from the website * The iRegulon plugin can also be used to query a TF-targets database made of ***high-confidence target genes*** predicted from the systematic analysis of thousands of cancer gene signatures. ![]() * New networks can be automatically generated based on the ***predicted TF-target interactions***. The ***Motif2TF*** associations are based on PWM annotation, the use of TF homology, and of motif similarity. * The output of iRegulon is a list of enriched motifs/tracks, alongside with candidate transcription factors. It allows detecting TFs using gene rankings according to the highest ChIP peak within the regulatory space using more than one thousand ChIP-Seq tracks. * ***Track discovery*** has been added in version 1.2. * ***Motif discovery*** is performed in proximal and distal sequences, across ten vertebrate genomes, using nearly 10 thousand candidate motifs (position weight matrices or PWMs). The iRegulon plugin allows you to identify regulons using motif and track discovery in an existing network or in a set of co-regulated genes. A regulon consists of a transcription factor (TF) and its direct transcriptional targets, which contain common TF binding sites in their cis-regulatory control elements. ![]()
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