【摘要】 目的分析不同人种乳腺癌的差异表达基因及关键蛋白调控基因与预后的关系。方法基于TCGA数据库中不同人种乳腺癌转录组表达谱来筛选差异表达基因,并进行基因本体论注释和京都基因与基因组百科全书(KEGG)富集分析。应用STRING数据库构建蛋白质互相作用网络,并在Cytoscape软件中进行可视化和模块挖掘,获取关键蛋白调控基因。结合对应的临床信息使用R软件对这些关键蛋白调控基因绘制生存曲线进行验证。结果共筛选出差异表达基因894个,其中上调基因875个,下调基因19个。差异表达基因主要与角化作用、表皮细胞分化等生物学过程有关,与角质化包膜、中间丝细胞骨架、角蛋白丝等细胞组分有关,与皮肤表皮的结构成分、葡萄糖醛酸转移酶活性等分子功能有关。KEGG通路主要与细胞色素P450代谢异种生物、戊糖和葡萄糖醛酸转换、化学致癌作用等有关。结论关键蛋白调控基因CASP14、MYF6、ALB与不同人种乳腺癌的发生和预后有紧密的关系,为精准治疗提供了新思路。更多还原

【Abstract】 Objective To analyze the relationship between differentially expressed genes and key protein regulatory genes of different races of breast cancer and the prognosis.Methods Based on the transcriptome expression profiles of different races of breast cancer in TCGA database, differentially expressed genes were screened, and gene ontology annotation and Kyoto gene and genome Encyclopedia(KEGG) enrichment analysis were performed.The protein-protein interaction network was constructed by STRING database, and the key protein regulatory genes were obtained by visualization and module mining in Cytoscape software.Combined with the corresponding clinical information, the survival curve of these key protein regulatory genes was drawn and verified by R software.Results A total of 894 differentially expressed genes were screened, including 875 up-regulated genes and 19 down-regulated genes.Differentially expressed genes were mainly related to biological pathways such as keratinization and epidermal cell differentiation, related to cellular components such as keratinized envelope, intermediate filament cytoskeleton and keratin filaments, and related to molecular functions such as structural components of skin epidermis and glucuronidase activity.KEGG pathway was mainly related to cytochrome P450 metabolism of xenobiotics, pentose and glucuronic acid conversion, chemical carcinogenesis and so on.Conclusion The key protein regulatory genes CASP14,MYF6 and ALB are closely related to the occurrence and prognosis of breast cancer in different races, and provide a new idea for precise treatment.更多还原