目的 初步寻找新的与肺癌相关的基因， 为全面揭开肺癌发病机制、进一步诊断和治疗肺癌提供依据。方法 ( 1)通过基因表达芯片筛选被动吸烟致小鼠肺癌中异常表达的基因;( 2)荧光实时定量PCR验证部分基因芯片结果;( 3)应用western blotting分析方法检测小鼠肺组织中Angiopoietin-3( Ang-3)基因的蛋白表达量变化。结果 实时荧光定量PCR结果显示Ang-3基因的mRNA相对表达量在肺癌组( 30.6544±15.2245)明显高于在正常对照组( 1.0469±0.3441， P<0.05)。Western blotting结果进一步表明吸烟导致Ang-3基因蛋白高表达( 1.2724±0.1493)， 尤其是在肺癌组织中( 1.5901±0.1189)明显高于正常肺组织中( 0.9054±0.0523)， 差异有统计学意义( P<0.05)。结论 Ang-3基因在被动吸烟所致小鼠肺癌的发生、发展中发挥一定的作用。

Objective To provide evidences for searching initially new correlated genes of lung cancer, and to reveal lung carcinogenesis, development and prognosis. Methods 1.To screen the genes of anomalous expression in mouse lung cancer induced by tobacco smoke through gene expression chip of mouse genome; 2.To identify the partial Results of gene chip by fluorescence-based real-time PCR; 3.To detecting the protein expression changes of Ang-3 in mouse lung cancer by western Blotting essay. Results Real-time PCR showed that Ang-3 gene presented higher expression in the tumor group ( 30.6544?15.2245)than in the control normal group( 1.0469?0.3441), P<0.05. Western blotting assay further indicated that smoking could upregulate the expression of Ang-3( 1.2724?0.1493); moreover, Ang-3 was overexpressed in lung cancer tissue ( 1.5901?0.1189)than in normal tisuue( 0.9054?0.0523), P<0.05. Conclusions Ang-3 gene plays an important role in mouse lung cancer induced by tobacco smoke.