吸烟肺腺癌患者关键基因的生物学分析

Bioinformatics analysis of key genes associated with lung adenocarcinoma in smoking patients

目的从基因水平揭示吸烟参与肺腺癌发病的机制,探索吸烟肺腺癌的关键基因,并进行生物学功能预测。方法从基因芯片公共数据库(GEO)中下载吸烟肺腺癌患者、非吸烟肺腺癌患者及正常对照组的相关基因芯片数据,将数据分为两组,一组为吸烟肺腺癌患者与正常对照;另一组为吸烟肺腺癌患者与非吸烟肺腺癌患者,利用GEO2R进行差异基因分析,筛选出两组中吸烟肺腺癌患者共同差异高表达基因,并采用DAVID数据库对差异高表达基因进行基因本体(GO)分析、京都基因与基因组百科全书(KEGG)及Pathway生物信息学分析。结果筛选出两组中吸烟肺腺癌患者共同差异高表达基因112个,其中主要是以极光激酶A(AURKA)基因、叉头框转录因子M1(FOXM1)基因、染色体结构维持蛋白2(SMC2)基因为核心的关键基因组,其生物学作用主要涉及细胞周期、p53信号通路及DNA复制等生物学通路。结论通过对吸烟肺腺癌患者的相关基因芯片数据进行生物信息学分析,提示吸烟对肺腺癌的发病是多基因作用的结果,其中AURKA、FOXM1、SMC2为吸烟肺腺癌患者组织中的核心关键基因,对其相关基因的进一步分析有利于揭示吸烟在肺腺癌患者中的分子生物学作用。

Objective To explore the key genes associated with lung adenocarcinoma in smoking patients by bioinformatics. Methods The microarray data of smoking and non-smoking patients with lung adenocarcinoma, and normal control were downloaded from the Gene Expression Omnibus(GEO) database. The data were divided into two groups, one included smoking patients with lung adenocarcinoma and normal control, the other included smoking and non-smoking patients with lung adenocarcinoma. GEO2R was used for online differential gene analysis to screen out common highly expressed genes in both groups. Then String and DAVID were used to conduct gene ontology(GO) analysis, Kyoto Encyclopedia of Genes and Genomes(KEGG) Pathway analysis, and bioinformatics analysis was performed on the highly expressed genes. Results A total of 112 differentially expressed genes of patients with lung adenocarcinoma were screened out, among which Aurora kinase A(AURKA), forkhead box protein M1(FOXM1) and structural maintenance of chromosomes 2(SMC2) were the core key genes.These genes were involved in the cell cycle, p53 signaling pathway and DNA replication signaling pathway. Conclusion Bioinformatics analysis of gene chip data of smoking patients with adenocarcinoma suggests that the onset of lung adenocarcinoma might be the result of multiple genes, and AURKA, FOXM1, SMC2 are the core key genes of smoking patients, further study on the related genes might shed light on the molecular biological role of smoking in patients with lung adenocarcinoma.