目的:利用基因芯片技术分析肝癌HepG2细胞和正常肝上皮L02细胞中miRNA的表达,并对HepG2细胞中低表达的miRNA-122a进行靶基因预测及相关生物信息学分析,为以miRNA-122a为靶点的基因治疗提供理论和实验基础。方法:利用基因芯片技术检测HepG2细胞和L02细胞中miRNA-122a表达水平,通过生物信息学预测miRNA-122a的靶基因,并对其靶基因进行功能富集分析(GO—analysis)、信号转导通路富集分析(Pathway—analysis)和蛋白质相互作用网络分析。结果:与L02细胞比较,miRNA-122a在HepG2细胞中呈低表达。miRNA-122a预测靶基因有1104个,其靶基因集合功能分别富集于碳水化合物生物合成、核苷酸代谢、细胞因子受体结合、细胞周期等生物学过程(P〈0.001);信号转导通路显著富集于JAK—STAT信号通路、Wnt信号通路、MAPK信号通路、ErbB信号通路、细胞周期等信号转导通路(P〈0.001)。结论:miRNA-122a在HepG2细胞中呈现低表达,miRNA-122a预测靶基因集合显著富集在与肿瘤发生相关的信号通路中。
Objective: The present study aimed to investigate miRNA expression patterns in hepatocellular carcinoma t nep~Jz and normol liver epithelial (LO2) cell lines. Another aim was to bioinformatically analyze as well as predict the target genes of miR-122a to provide both theoretical and experimental basis for gene therapy. Methods: The expression levels of miRNA-122a in HepG2 and LO2 cells were detected using the gene chip technology. The bioinformatic analysis of the target genes of miRNA-122a involved enrichment ( gene ontology ), signal transduction pathway enrichment, and protein interaction network analyses. Results: miRNA-122a expression significantly decreased in HepG2 cells, compared with LO2 cells. The number of miRNA-122a target genes was 1104. The functions of these target genes were enriched in carbohydrate biosynthesis, nucleotide metabolism, cytokine receptor binding, cell cycle, and other biological processes ( P 〈 0.001 ). The JAK-STAT signaling, Writ signaling, MAPK signaling, ErbB signaling, and cell cycle signal transduction pathways were significantly enriched ( P 〈 0.001 ). Conclusion: miRNA-122a expression significant- ly decreased in HepG2 cells. Some of the predicted target genes of miRNA-122a were significantly enriched in tumor related with sig- naling pathways.