中文摘要：

目的对hsa-miR-138进行靶基因、功能富集分析（GO分析）、信号通路富集分析及转录因子预测等生物信息学分析,为后续深入研究hsa-miR-138功能提供实验验证的理论基础。方法通过UCSC基因组浏览器、Target Scan、starbase、DAVID及KEGG公共数据库、Chipbase等在线工具分析hsa-miR-138序列,预测hsa-miR-138-1的靶基因,对预测的靶基因进行GO分析和信号通路富集分析,预测hsa-miR-138的可能转录调控因子。结果 hsa-miR-138序列在各物种间具有高度保守性。通过对目前文献的检索,发现hsa-miR-138-1的靶基因中既有抑癌基因,也有癌基因。GO分析发现hsa-miR-138-1靶基因主要富集在转录调控、转录、RNA代谢过程的调节、基因表达、生物大分子的合成等方面（P〈0.01）,KEGG通路分析提示相关信号通路主要涉及癌症通路、轴突导向、细胞内噬作用、Wnt信号转导、神经营养因子信号转导等重要生理病理过程。应用Chipbase预测出hsamiR-138的19个调控转录因子。结论 hsa-miR-138可能参与多种重要的生物学过程,并作为双向调节因子调控肿瘤的生物学行为。

英文摘要：

Objective To predict target genes of hsa-miR-138 by bioinformatic analysis,carry out functional enrichment analysis and signal pathway enrichment analysis of the target genes,and explore its transcriptional regulatory factors,so as to provide a theoretical basis for the further study of hsa-miR-138 function. Methods The sequences of hsa-miR-138 were analyzed with UCSC,and hsa-miR-138-1 target genes were predicted using TargetS can,starbase. Functional enrichment analysis of target genes and signal pathway enrichment analysis were carried out using DAVID and KEGG database. Chipbase was used to predict the possible transcriptional regulatory factors of hsa-miR-138. Results The sequence of hsa-miR-138 was highly conserved among various species. By searching the current literatures,the target genes of hsa-miR-138-1 were found to be not only tumor suppressor genes,but also cancer genes. GO analysis showed that the target genes of hsa-miR-138-1 were mainly enriched in transcription regulation,transcription,RNA metabolism,gene expression,biological macromolecular synthesis（P〈0.01）,and KEGG pathway analysis indicated that the related signaling pathways were involved in the physiological and pathological processes,including cancer pathway,axon guidance,endocytosis,Wnt signaling pathway,neurotrophin signaling pathway. A total of 19 regulatory transcription factors of hsa-miR-138 were predicted by Chipbase. Conclusion hsa-miR-138 may be involved in some important biological processes,which act as a bilateral regulative factor for tumor biological behavior.