中文摘要：

目的 探讨miR-622对H460肺癌细胞增殖的影响及其作用机制.方法 利用脂质体瞬时转染方法将miR-622模拟物及其对照核苷酸转染至肺癌细胞内.miRNA定量试剂盒检测miR-622的表达.CCK-8试剂盒检测细胞增殖.生物信息学分析miR-622的靶点.蛋白印迹方法检测K-Ras蛋白的表达.构建含K-Ras mRNA的3非翻译区的报告基因载体,检测萤火虫/Renilla荧光素酶活性.结果 转染miR-622模拟物可提高miR-622的表达,并使H460和16HBE-T的细胞增殖率分别降至（58.60±4.27）％和（65.17±4.67）％,P均＜0.01.生物信息学分析K-Ras为miR-622的一潜在靶点.转染miR-622模拟物可明显抑制K-Ras蛋白的表达.共转染miR-622模拟物和K-Ras-3＇UTR报告基因,可使萤火虫/Renilla荧光素酶的活性降低至（60.22±2.50）％.结论 miR-622可通过负性调控靶点K-Ras抑制肺癌细胞的增殖.

英文摘要：

Objective To investigate the effect of miR-622 on proliferation of H460 cell. Methods The miR-622 mimic were transiently transfected into H460 lung cancer cells to elevate the level of miR-622. The expression level of miR-622 was quantified by Real-time quantitative PCR. CCK-8 assay was used to detect the cell proliferation. We used bioinformatics tools to predict target mRNA formiR-622. Western blot was employed to detect the K-Ras protein level. We constructed the reporter gene plasmid carrying 3＇ UTR of K-Ras Mrna to check the activity of reporter gene. Results The elevating expression level of miR-622 significantly decreased cell proliferation ratio to （58. 60 ±4. 27）% and （65. 17 ±4. 67）%, separately in H460 and 16HBE-T cells, both P 〈 0. 01. The K-Ras mRNA was a putative target for miR-622. The elevating expression level of miR-622 significantly reduced the K-Ras protein level Co-transfecting miR-622 mimic and reporter geneplasmid for K-Ras 3＇UTR de- creased the luciferase activity to （60. 22 ＋ 2. 50） %, P 〈 0. 01. Conclusion miR-622 inhibits the proliferation of lung cancer cell through targeting K-Ras.