目的 充分挖掘生物信息学数据库,筛选可与长链非编码RNA(long non-coding RNA,lncRNA)PURPL结合的微小RNA(microRNA,miRNA)及下游靶基因和信号通路,进而构建PURPL/miRNA/靶基因/信号通路调控网络,为后续研究PURPL参与卵巢癌细胞侵袭和转移的分子机制奠定基础.方法 基于lncRNA/miRNA调控机制,多数据库交叉预测可与PURPL结合的下游miRNA及其靶基因,并对靶基因进行蛋白质互作网络分析和核心蛋白筛选,进而行基因本体(gene ontology,GO)、疾病和京都基因和基因组百科全书(Kyoto Encyclopedia of Genes and Genomes,KEGG)信号通路富集分析.结果 PURPL在正常组织和癌组织(包括正常卵巢组织和卵巢癌组织)中存在差异化表达,筛选出3个下游miRNA及其341个靶基因,经过蛋白质互作网络分析、富集分析,筛选出15个核心基因,最终确定了 PURPL、下游3个miRNA、15个核心靶基因及潜在信号通路组成的调控网络.结论 PURPL/miRNA/靶基因/信号通路调控网络可为后续卵巢癌侵袭和转移的分子机制研究提供潜在的分子靶点.
Bioinformatics Analysis of miRNA/mRNA Network Regulated by Long Non-coding RNA PURPL
Objective To screen microRNA(miRNA)that could bind to long non-coding RNA(lncRNA)p53 upregulated regu-lator of p53 levels(PURPL),and downstream target genes and signaling pathways by comprehensive bioinformatics database mining,con-struct PURPL/miRNA/target genes/signaling pathways regulatory network,and provide foundation for further study on the molecular mechanism of PURPL involved in the invasion and metastasis of ovarian cancer cells.Methods Based on the lncRNA/miRNA regulatory mechanism,using multi-database to cross-predict the downstream miRNA that could bind to PURPL,and target genes for miRNA.Protein-protein interaction(PPI)network analysis and core protein screening for target gene transcription proteins were conducted.Fi-nally,core genes were analyzed by gene ontology(GO),disease and Kyoto Encyclopedia of Genes and Genomes(KEGG)signaling path-ways enrichment analysis.Results PURPL were differentially expressed in normal tissues and cancer tissues(including normal ovarian tissues and ovarian cancer tissues).The 3 downstream miRNA and 341 target genes were screened,and 15 core genes were screened out through PPI network analysis and enrichment analysis.Finally,the regulatory network composed of PURPL,3 downstream miRNA,15 core target genes and potential signaling pathways was determined.Conclusion PURPL/miRNA/target genes/signaling pathways regula-tory network might provide potential molecular targets for the subsequent molecular mechanism research for the invasion and metastasis of ovarian cancer.
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