为研究miR-520c-3p对肺癌细胞增殖和凋亡的影响及其潜在的作用机制，用实时定量RT-PCR检测肺癌细胞H1299、NCI-H460、A549和正常肺上皮细胞BEAS-2B中miR-520c-3p和MEX3同源物A（MEX3 homolog A，MEX3A）的表达水平。将miR-NC、miR-520c-3p、si-NC、si-MEX3A、anti-miR-NC、anti-miR-520c-3p转染至H1299细胞后，用细胞计数试剂盒8（cell counting kit 8，CCK-8）法检测细胞增殖，流式细胞术检测细胞凋亡，Western blotting检测蛋白表达，双荧光素酶报告基因检测实验检测细胞的荧光活性。结果显示，与正常肺上皮细胞BEAS-2B比较，肺癌细胞H1299、NCI-H460、A549中miR-520c-3p的表达水平均显著降低（P < 0.05），MEX3A mRNA和蛋白的表达水平显著升高（P < 0.05）。miR-520c-3p过表达、MEX3A抑制表达均可抑制H1299细胞的增殖活力，促进细胞凋亡；miR-520c-3p过表达抑制CyclinD1、Bcl-2蛋白的表达，促进p21、Cleaved Caspase-3、Bax蛋白的表达；MEX3A抑制表达抑制CyclinD1、Bcl-2蛋白的表达，促进p21、Bax蛋白的表达。miR-520c-3p可靶向调控MEX3A的表达；MEX3A过表达逆转了miR-520c-3p过表达对肺癌细胞H1299的增殖抑制和凋亡促进作用。提示miR-520c-3p可抑制肺癌细胞H1299的增殖，促进其凋亡，其机制可能与靶向MEX3A有关，这将为肺癌的预防和治疗提供新靶点。

To investigate the effect of miR-520c-3p on proliferation and apoptosis of lung cancer cell and its mechanism, real-time quantitative RT-PCR was used to detect the expression of miR-520c-3p and MEX3 homolog A (MEX3A) in lung cancer cells H1299, NCI-H460, A549 and normal lung epithelial cell BEAS-2B. After miR-NC, miR-520c-3p, si-NC, si-MEX3A, anti-miR-NC, anti-miR-520c-3p were transfected into H1299 cells, the cell proliferation was detected by cell counting kit 8（CCK-8） method; the apoptosis was detected by flow cytometry; the protein expression was detected by Western blotting; fluorescence activity of cells was detected by dual luciferase reporter assay. The results showed that, compared with the normal lung epithelial cell BEAS-2B, the expression of miR-520c-3p in lung cancer cells H1299, NCI-H460 and A549 was significantly decreased (P < 0.05), in the contrast, the expression of MEX3A mRNA and protein were significantly increased (P < 0.05). Overexpression of miR-520c-3p and decreased expression of MEX3A inhibited the proliferation, and promoted apoptosis of H1299 cells. Overexpression of miR-520c-3p inhibited the expressions of CyclinD1 and Bcl-2 proteins, and promoted the expressions of p21, Cleaved Caspase-3 and Bax proteins; inhibition of MEX3A inhibited the expressions of CyclinD1 and Bcl-2 proteins, and promoted the expressions of p21 and Bax proteins. miR-520c-3p can specifically regulate the expression of MEX3A; MEX3A overexpression reversed the effect of overexpressed miR-520c-3p on proliferation inhibition and apoptosis promotion of lung cancer cells H1299. Taken together, these results indicate that miR-520c-3p could inhibit the proliferation and promote the apoptosis of lung cancer cell H1299 by targeting MEX3A. These findings will provide a new target for the prevention and treatment of lung cancer.