目的:探讨miR-623调控非小细胞肺癌细胞A549凋亡的潜在分子机制。方法:在非小细胞肺癌细胞A549中过表达或抑制miR-623，检测细胞的凋亡水平。通过miRDB在线分析和荧光素酶报告系统分析miR-623的底物。通过siRNA和质粒分别敲低和过表达底物，检测非小细胞肺癌细胞A549的凋亡水平。结果:过表达miR-623后，非小细胞肺癌细胞A549的凋亡水平下降(n t＝3.313，n P0.05)。n 结论:miR-623通过靶向DNM2 mRNA的3′端非编码区，抑制了DNM2的表达，最终抑制了非小细胞肺癌细胞A549的凋亡。“,”Objective:To investigate the potential molecular mechanism of miR-623 regulating the apoptosis of non-small cell lung cancer cell A549.Methods:miR-623 was overexpressed or knocked down in non-small cell lung cancer cell A549 to detect the level of apoptosis.The substrate of miR-623 was analyzed by miRDB online analysis and luciferase reporting system.SiRNA and plasmid were used to knock down and overexpress the substrate, respectively, and the apoptosis level of non-small cell lung cancer cell A549 was detected.Results:After overexpression of miR-623, the apoptotic level of non-small cell lung cancer cell A549 decreased (n t=3.313, n P0.05).n Conclusions:miR-623 inhibits the translation of DNM2 by targeting the 3′non-coding region of DNM2 mRNA, and finally inhibits the apoptosis level of non-small cell lung cancer cell A549.