Screening of core genes and prediction of ceRNA regulation mechanism of circRNAs in nasopharyngeal carcinoma by bioinformatics analysis.

IF 2.3 4区 医学 Q3 ONCOLOGY
HongMin Chen, XiaoXiao Shi, Li Ren, YuMing Wan, HongYu Zhuo, Li Zeng, WangMu SangDan, Feng Wang
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引用次数: 0

Abstract

Background: Nasopharyngeal carcinoma (NPC) represents a highly aggressive malignant tumor. Competing endogenous RNAs (ceRNA) regulation is a common regulatory mechanism in tumors. The ceRNA network links the functions between mRNAs and ncRNAs, thus playing an important regulatory role in diseases. This study screened the potential key genes in NPC and predicted regulatory mechanisms using bioinformatics analysis. Methods: The merged microarray data of three NPC-related mRNA expression microarrays from the Gene Expression Omnibus (GEO) database and the expression data of tumor samples or normal samples from the nasopharynx and tonsil in The Cancer Genome Atlas (TCGA) database were both subjected to differential analysis and Weighted Gene Co-expression Network Analysis (WGCNA). The results from two different databases were intersected with WGCNA results to obtain potential regulatory genes in NPC, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses. The hub-gene in candidate genes was discerned through Protein-Protein Interaction (PPI) analysis and its upstream regulatory mechanism was predicted by miRwalk and circbank databases. Results: Totally 68 upregulated genes and 96 downregulated genes in NPC were screened through GEO and TCGA. According to WGCNA, the NPC-related modules were screened from GEO and TCGA analysis results, and the genes in the modules were obtained. After the results of differential analysis and WGCNA were intersected, 74 differentially expressed candidate genes associated with NPC were discerned. Finally, fibronectin 1 (FN1) was identified as a hub-gene in NPC. Prediction of upstream regulatory mechanisms of FN1 suggested that FN1 may be regulated by ceRNA mechanisms involving multiple circRNAs, thereby influencing NPC progression through ceRNA regulation. Conclusion: FN1 is identified as a key regulator in NPC development and is likely to be regulated by numerous circRNA-mediated ceRNA mechanisms.

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生物信息学分析鼻咽癌circRNAs核心基因筛选及ceRNA调控机制预测
背景:鼻咽癌是一种高度侵袭性的恶性肿瘤。竞争内源性rna (Competing endogenous RNAs, ceRNA)调控是肿瘤中常见的调控机制。ceRNA网络连接mrna和ncrna之间的功能,因此在疾病中起着重要的调节作用。本研究利用生物信息学方法筛选鼻咽癌的潜在关键基因,并预测鼻咽癌的调控机制。方法:将基因表达Omnibus (Gene expression Omnibus, GEO)数据库中3个npc相关mRNA表达的微阵列数据与癌症基因组图谱(Cancer Genome Atlas, TCGA)数据库中来自鼻咽部和扁桃体的肿瘤样本或正常样本的表达数据进行差异分析和加权基因共表达网络分析(Weighted Gene Co-expression Network analysis, WGCNA)。将来自两个不同数据库的结果与WGCNA结果交叉,获得NPC的潜在调控基因,然后进行基因本体(GO)和京都基因与基因组百科全书(KEGG)功能富集分析。通过蛋白-蛋白相互作用(Protein-Protein Interaction, PPI)分析确定候选基因中的hub基因,并通过miRwalk和circbank数据库预测其上游调控机制。结果:通过GEO和TCGA共筛选到鼻咽癌中68个上调基因和96个下调基因。根据WGCNA,从GEO和TCGA分析结果中筛选npc相关模块,获得模块中的基因。将差异分析结果与WGCNA交叉分析后,鉴定出74个与鼻咽癌相关的差异表达候选基因。最后,纤维连接蛋白1 (FN1)被鉴定为鼻咽癌的中心基因。对FN1上游调控机制的预测表明,FN1可能受到涉及多个circrna的ceRNA机制的调控,从而通过ceRNA调控影响NPC的进展。结论:FN1被认为是鼻咽癌发展的关键调节因子,并可能受到多种circrna介导的ceRNA机制的调节。
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来源期刊
CiteScore
6.30
自引率
0.00%
发文量
134
审稿时长
4-8 weeks
期刊介绍: Pathology & Oncology Research (POR) is an interdisciplinary Journal at the interface of pathology and oncology including the preclinical and translational research, diagnostics and therapy. Furthermore, POR is an international forum for the rapid communication of reviews, original research, critical and topical reports with excellence and novelty. Published quarterly, POR is dedicated to keeping scientists informed of developments on the selected biomedical fields bridging the gap between basic research and clinical medicine. It is a special aim for POR to promote pathological and oncological publishing activity of colleagues in the Central and East European region. The journal will be of interest to pathologists, and a broad range of experimental and clinical oncologists, and related experts. POR is supported by an acknowledged international advisory board and the Arányi Fundation for modern pathology.
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