中文摘要：

目的 探讨反式-7,8-二羟-9,10-环氧苯并芘（anti-BPDE）诱导恶变的人支气管上皮细胞（16HBE-T）中miR-542-3p在细胞恶性转化中的作用.方法 运用实时荧光定量PCR法验证miR-542-3p成熟体在16HBE-T和非转化对照细胞（16HBE-N）中的表达水平.瞬时转染化学合成的miR-542-3p模拟物上调16HBE-T的miR-542-3p成熟体表达水平,检测miR-542-3p表达水平改变对16HBE-T细胞的增殖能力、细胞周期、细胞凋亡、软琼脂克隆形成率及细胞迁移能力的影响.结果 转染前16HBE-T中miR-542-3p成熟体表达水平是16HBE-N的（39.08±6.95）%（t=15.18,P＜0.05）.瞬时转染化学合成的miR-542-3p模拟物上调16HBE-T的miR-542-3p成熟体表达水平后,16HBE-T中miR-542-3p成熟体表达水平是转染前的（5.23±0.55）倍（t=17.37,P＜0.05）.miR-542-3p模拟物组（mimic组）与16HBE-T组（100%）相比,增殖率下降到（62.06±5.61）%（t=-17.28,P＜0.05）,G0/G1期比例上升到（74.76±4.86）%（t=4.53,P＜0.05）,克隆形成率降低为（5.87±0.67）%（t=-6.66,P＜0.05）.mimic组生长细胞覆盖区面积比（0.31±0.08）明显降低（t=-6.78,P＜0.05）,凋亡无改变.结论 miR-542-3p表达水平升高会降低anti-BPDE恶性转化细胞的增殖能力和恶性程度,推断miR-542-3p是类抑癌基因,在anti-BPDE诱导致癌过程中低表达的miR-542-3p可能是促成恶性转化的重要因素.

英文摘要：

Objective To explore the effect of miR-542-3p in malignant transformation of human bronchial epithelial cells （16HBE） induced by anti-benzo（a） pyrene-7,8-diol-9, 10-epoxide （anti-BPDE）.Methods The relative expression level of mature miR-542-3p in transformed cells （16HBE-T） and untransformed control cells （16HBE-N） was measured by real-time quantitative polymerase chain reaction （qRT-PCR）. miRNA mimic was transiently transfected into 16HBE-T to change the expression level of miR-542-3p,and then the influenced changes of cell proliferation,cell cycle, apoptosis, and soft agar colony formation rate and the migration of transfected cells were analyzed. Results Before transfection, the expression level of mature miR-542-3p in 16HBE-T was lower （39. 08 ± 6. 95 ） % than it in 16HBE-N （ t =15. 18,P〈 0.05）. In comparison with the 16HBE-T group, the expression level of miR-542-3p in miR-542-3p mimic-transfected group was （ 5.23 ± 0. 55 ） fold （ t = 17. 37, P 〈 0. 05 ） after transfection. Cell proliferation of mimic-transfected group was decreased to （ 62. 06 ± 5. 61 ） % （ t = - 17. 28, P 〈 0. 05 ）,percentage of cells in G0/G1 phase up to （ 74. 76 ± 4. 86 ） % （ t = 4. 53, P 〈 0. 05 ）, rate of colony formation degrade to（5.87 ± 0. 67 ） % （ t = - 6. 66, P 〈 0. 05 ）, coverage areas ratio decreased to （0. 31 ± 0. 08 ） （ t =-6. 78 ,P 〈0. 05 ）. There was no change with apoptosis. Conclusion Our studies showed that miR-542-3p played the role as a tumor suppressor, which led to a significant decrease in the proliferation capacity and degree of malignancy. These findings suggest aberrantly down-regulated miR-542-3p may be one critical factor that contributes to malignant transformation of 16HBE induced by anti-BPDE.