大鼠C6脑胶质瘤模型的基因表达谱分析

Gene expression profile analysis of rat model of intracranial C6 glioma

目的:筛选和分析大鼠胶质瘤模型与正常星型胶质细胞中的差异表达基因。方法:构建大鼠C6颅内胶质瘤模型,利用Illumina Hi Seq 4000技术对大鼠胶质瘤模型的胶质细胞和正常星形胶质细胞进行转录组测序并对测序结果进行功能注释。以q值<0. 05为标准筛选差异表达基因,并通过GO和KEGG数据库分析其功能和参与的信号通路。结果:较之正常星形胶质细胞,大鼠胶质瘤模型组细胞共筛选得到9221个差异表达基因,其中4604个基因表达上调,4617个基因表达下调; GO富集结果表明:这些差异表达基因共映射到575个GO term,与各类结合相关的分子如蛋白结合、离子结合、小分子结合、核苷酸结合等功能富集显著; KEGG富集结果表明:差异表达基因共参与22条通路,富集最多的是癌症发生通路、MAPK通路、胞吞通路和黏着斑通路。结论:成功获取大鼠胶质瘤模型细胞与正常胶质细胞的基因表达谱,差异表达基因富集在癌症发生通路、MAPK通路、胞吞作用通路和黏着斑等生物学通路,这些信号通路可能在胶质瘤发生发展过程中发挥重要作用,对其进一步分析将为临床治疗胶质瘤提供新的靶点。

Objective： To screen and analyze the differentially expressed genes between rat model of intracranical C6 glioma cells and normal astrocytes.Methods： The RNA of rat model of intracranial C6 glioma cells and normal astrocytes were sequenced using Illumina Hi Seq 4000 and its results were annotated and analyzed with the Kyoto Encyclopedia of Genes and Genomes（ KEGG）,Gene Ontology（ GO） database.The logarithm used to identify the differentially expressed genes was q values 0.05.Results： A total of 9221 differentially expressed genes were screened from rat glioma cells Compared with normal astrocytes,4604 genes were up-regulated and 4617 genes were down-regulated.GO enrichment results showed that differentially expressed genes were mapped to 575 GO terms,which were mainly related to the molecular function of binding such as protein binding,ion binding,small molecule binding,and nucleotide binding.KEGG enrichment results showed that differentially expressed genes were involved in 22 patways and the most relevant biological pathways are pathways in cancer,MAPK signaling,endocytosis and focal adhesion.Conclusion： The gene expression profiles of cell from rat glioma model and normal astrocytes were obtained successfully,and differentially expressed genes were annotated by GO and KEGG,differentially expressed genes mainly involved in the biological pathways like pathways in cancer,MAPK signaling,endocytosis and focal adhesion.These pathways may play importantroles in the development of glioma.Further analysis will provide new targets for clinical prevention and treatment of glioma.