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目的:探讨n K-ras基因对PMn 2.5染毒人支气管上皮（HBE）细胞部分癌基因和抑癌基因表达的影响。n 方法:于2019年9月，根据n K-ras基因mRNA序列，设计合成干扰序列，转染HBE细胞构建n K-ras基因沉默细胞。用10、50 μg/ml PMn 2.5混悬液及10 μmol/L Crn 6+分别染毒HBE细胞和n K-ras基因沉默细胞，实时荧光定量PCR检测n c-myc、n c-fos、n N-ras、n cyclin-D1、n p16、n p53基因的mRNA表达水平，Western blot检测c-myc和p53蛋白表达水平。n 结果:K-ras基因沉默细胞中n K-ras基因mRNA表达水平下降（80.5%±3.6%），K-ras蛋白表达水平下降（58.9%±4.7%）（n P<0.01）。各浓度PMn 2.5染毒HBE细胞组、n K-ras沉默细胞组及10 μmol/L Crn 6+染毒HBE细胞组、n K-ras沉默细胞组n c-myc、n c-fos、n N-ras、n cyclin-D1基因mRNA表达水平均高于未染毒相应细胞对照组，n p16和n p53基因mRNA表达水平低于未染毒相应细胞对照组（n P<0.01）；10 μg/ml PMn 2.5染毒n K-ras沉默细胞组n c-myc、n c-fos、n p16基因mRNA表达水平低于10 μg/ml PMn 2.5染毒HBE细胞组，n p53基因mRNA表达水平高于10 μg/ml PMn 2.5染毒HBE细胞组（n P<0.01）；50 μg/ml PMn 2.5染毒n K-ras沉默细胞组n c-fos、n N-ras、n cyclin-D1、n p16和n p53基因mRNA表达水平均低于50 μg/ml PMn 2.5染毒HBE细胞组（n P<0.01）。50 μg/ml PMn 2.5染毒HBE细胞组c-myc蛋白表达水平高于未染毒HBE细胞组，p53蛋白表达水平低于未染毒HBE细胞组（n P<0.05）；50 μg/ml PMn 2.5染毒n K-ras沉默细胞组c-myc蛋白表达水平高于未染毒n K-ras沉默细胞组（n P<0.05）。n 结论:PMn 2.5可引起HBE细胞癌基因表达升高，n K-ras基因沉默能抑制PMn 2.5诱导HBE细胞癌基因的表达。n “,”Objective:To explore the effects of n K-ras gene on the expressions of oncogenes and cancer suppressor genes in human bronchial epithelial (HBE) cells which were exposed to PMn 2.5.n Methods:According to the mRNA sequence of n K-ras gene provided by GenBank in September 2019, interference sequences were designed and synthesized, and the recombinant lentiviral vector was transfected into HBE cell to construct the n K-ras gene-silenced cells. HBE cells and n K-ras gene-silenced cells were exposed to 10 μg/ml, 50 μg/ml PM n 2.5 suspension and 10 μmol/L Cr n 6+. Real-time fluorescent quantitative PCR was used to detect the mRNA expression levels of n c-myc, n c-fos, n N-ras, n cyclin-D1, n p16 and p53 genes, the expression levels of p53 and c-myc proteins were detected by Western blot.n Results:In n K-ras silenced cell group, n K-ras mRNA expression level decreased (80.5%±3.6%) and K-ras protein level decreased (58.9%±4.7%) when compared with the control group (n P<0.01) . Compared with the correspoding cell control group without exposure, the mRNA expression levels ofn c-myc, n c-fos, n N-ras and cyclin-D1 genes in HBE cell group exposed to different concentrations of PMn 2.5, n K-ras silenced cell group exposed to different concentrations of PMn 2.5, HBE cell group exposed to 10 μmol/L Cr n 6+ and n K-ras silenced cell group exposed to 10 μmol/L Cr n 6+ were increased, the mRNA expressions of n p16 and p53 genes were decreased (n P<0.01) . Compared with HBE cell group exposed to 10 μg/ml PMn 2.5, the mRNA expressions of n c-myc, n c-fos and p16 genes in n K-ras silenced cells exposed to 10 μg/ml PM n 2.5 were decreased, and the n p53 mRNA level was increased (n P<0.01) . Compared with HBE cell group exposed to 50 μg/ml PMn 2.5, the mRNA expression levels of n c-fos, n N-ras, n cyclin-D1, n p16 and n p53 genes in n K-ras silenced cell group exposed to 50 μg/ml PM n 2.5 were decreased (n P<0.01) . Compared with the HBE cell group without exposure, c-myc protein increased and p53 protein decreased in HBE cells exposed to 50 μg/ml PMn 2.5 (n P<0.05) . Compared with then K-ras silenced cell group without exposure, c-myc protein increased in n K-ras silenced cells exposed to 50 μg/ml PM n 2.5 (n P<0.05) .n Conclusion:PMn 2.5 can increase the expression levels of oncogenes in HBE cells, and n K-ras gene silencing can inhibit the expression levels of oncogenes in HBE cells treated with PMn 2.5.n