目的:探讨切除修复交叉互补基因1(ERCC1)调节卵巢癌耐药株A2780/顺铂(DDP)细胞迁移及侵袭能力的作用及其机制。方法:根据细胞对顺铂的耐药性，分为普通组A2780、顺铂耐药组A2780/DDP。细胞计数试剂盒(CCK-8)检测A2780、A2780/DDP细胞活性及顺铂耐药性。Transwell细胞迁移、侵袭实验检测A2780、A2780/DDP细胞的迁移和侵袭能力。蛋白质印迹法(Western blot)检测A2780、A2780/DDP细胞中ERCC1、上皮表型E-钙黏蛋白(E-cadherin)及间质表型波形蛋白(Vimentin)的表达。小干扰RNA(siRNA)-ERCC1转染A2780/DDP中ERCC1表达后，Transwell细胞迁移、侵袭实验检测细胞迁移和侵袭能力的改变，Western blot检测细胞中ERCC1、E-cadherin及Vimentin表达的改变。两组间比较采用Student’s-n t检验。n 结果:A2780/DDP的半抑制浓度(ICn 50)值为17.66 mg/L，A2780的ICn 50值为2.236 mg/L，A2780/DDP较A2780的ICn 50提高了7.898倍。A2780/DDP细胞的迁移和侵袭能力明显高于非耐药株，且A2780/DDP中ERCC1和间质表型Vimentin的表达明显高于非耐药株A2780，而上皮表型E-cadhetin表达明显低于A2780。干扰A2780/DDP中ERCC1表达后，细胞的迁移和侵袭能力明显低于对照组，且细胞中ERCC1和间质表型Vimentin的表达低于对照组，而上皮表型E-cadhetin表达高于对照组。结果差异均有统计学意义。n 结论:A2780/DDP中高表达的ERCC1通过促进细胞发生上皮-间充质转化增强细胞的迁移及侵袭的能力。“,”Objective:To investigate the effect and mechanism of excision repair cross-complementation gene group 1 (ERCC1) in regulating cell migration and invasion of cisplatin-resistant ovarian cancer A2780/cisplatin (DDP) cells.Methods:According to the resistance of cells to cisplatin, the cells were divided into normal group A2780 and cisplatin resistance group A2780/DDP. Cell activity and cisplatin resistance of A2780 and A2780/DDP were detected by cell counting kit-8 (CCK-8). Transwell assay was used to detect the migration and invasion ability of A2780 and A2780/DDP cells. The expression of ERCC1, epithelial phenotype E-cadherin and mesenchymal phenotype Vimentin in A2780 and A2780/DDP cells was detected by Western blotting. After transfection of small interfering RNA (siRNA)-ERCC1 in A2780/DDP, Transwell cell migration and invasion assay was used to detect changes in cell migration and invasion ability, and Western blotting was used to detect changes in ERCC1, E-Cadherin and Vimentin expression. Student′s S-n T test was used for comparison between the two groups.n Results:Experiments showed that The the half inhibitory concentration (ICn 50) of A2780/DDP cells was 17.66 mg/L, and that of A2780 cells was 2.236 mg/L. The ICn 50 of the former was 7.898 times higher than that of the latter. Meanwhile, the migration and invasion ability of A2780/DDP cells was significantly higher than that of A2780 cells, and the expression of ERCC1 and mesenchymal phenotype Vimentin in A2780/DDP cells was significantly increased, while the expression of epithelial phenotype E-cadhetin was significantly decreased. After ERCC1 gene-specific interference in A2780/DDP cells, the ability of cell migration and invasion was significantly reduced. At the same time, the expression of ERCC1 and mesenchymal phenotype Vimentin in cells was down-regulated, and that of epithelial phenotype E-cadhetin was up-regulated. The results were statistically different.n Conclusion:The high expression of ERCC1 in A2780/DDP cells enhanced the ability of cell migration and invasion by promoting the formation of epithelial-mesenchymal transitions.