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目的:对胰腺癌细胞差异miRNAs表达谱进行生物信息学分析,以期从整体水平揭示microRNA在胰腺癌癌变和进展中的作用。方法:采用含有924条探针的microRNA微阵列检测胰腺癌Panc-1细胞,以3T3成纤维细胞为对照,筛选Panc-1细胞特异性microRNA表达谱;然后对上调和下调microRNA的靶基因进行Gene Ontology、Pathway和TFBS转录因子结合位点分析,以及构建microRNA和靶基因相互作用网络。结果:与3T3成纤维细胞的microRNA表达谱比较,筛选出9个Panc-1上调microR-NA,20个下调microRNA。TargetScan和mi-Randa软件预测出1 166个microRNA靶基因在Panc-1细胞中上调,212个靶基因下调。以上靶基因在DNA代谢、细胞间信号和胞质溶胶3种GO中富集显著;靶基因共涉及50条信号通路,其中富集度P<0.05的信号通路有6条;转录因子结合位点分析表明,CEBP-β、NF-κB和p53等对于上调以及下调的microRNA可能都有调节作用;microRNA和靶基因的相互作用网络分析表明,HIF-1A等基因连接度高。结论:利用生物信息学方法对胰腺癌细胞microRNA表达谱进行数据分析,可以为进一步了解胰腺癌的发病机制提供新的思路。
OBJECTIVE: To perform bioinformatics analysis of differentially expressed miRNAs in pancreatic cancer cells in order to reveal the role of microRNA in the carcinogenesis and progression of pancreatic cancers from the overall level. Methods: Panc-1 cells were detected by microRNA microarray with 924 probes. Panc-1 cell-specific microRNA expression profiles were screened by 3T3 fibroblasts. Gene targets of up-regulated and down- Ontology, Pathway and TFBS transcription factor binding site analysis, as well as the construction of microRNA and target gene interaction network. Results: Compared with 3T3 fibroblasts microRNA expression profiles, 9 Panc-1 up-regulated microR-NA and 20 down-regulated microRNAs. TargetScan and mi-Randa software predicted that 1,166 microRNA target genes were up-regulated in Panc-1 cells and 212 target genes were down-regulated. The above target genes were significantly enriched in DNA metabolism, intercellular signal and cytosolic GO. The target genes involved a total of 50 signal pathways, of which 6 were signaling pathways with enrichment P <0.05. The transcription factor binding sites Analysis showed that CEBP-β, NF-κB and p53 may regulate both up-regulated and down-regulated microRNAs. The network analysis of the interaction between microRNAs and target genes showed that HIF-1A and other genetic connections are high. Conclusion: Using bioinformatics methods to analyze the microRNA expression profile of pancreatic cancer cells may provide a new idea for further understanding the pathogenesis of pancreatic cancer.