目的 探讨慢病毒载体介导的RNA沉默CD55基因抑制胰腺癌BxPC-3细胞迁移、侵袭和成瘤的效果及机制.方法 采用CD55-RNAi-LV(慢病毒包装靶向抑制CD55的shRNA载体)转染BxPC-3细胞(实验组),设转染NC-GFP-LV(慢病毒包装作对照的空载体)的BxPC-3细胞为对照组,未转染的BxPC-3细胞为空白组.Transwell法检测各组细胞体外迁移、侵袭能力.三组细胞分别以1.0×107/200 μL的浓度注入裸鼠皮下,7周观察成瘤情况.结果 与对照组及空白组比较,实验组细胞迁移能力及侵袭能力明显减弱(P均＜0.05)；瘤体出现晚且瘤体体积小(P＜0.05).结论 CD55基因对胰腺癌细胞系BxPC-3细胞迁移、侵袭和成瘤能力有调控作用,可望成为胰腺癌新的治疗靶点.%Objective To investigate the specific silencing effect of lentiviral vector-mediated RNA interference targeting CD55 on cell migration, cell aggression and tumor formation in human pancreatic cancer cell line BxPC-3. Methods The lentiviral vector-mediated shRNA targeting CD55 was transfected into BxPC-3 cells. The BxPC-3 cells transfected with the lentiviral vector-CD55 -shRNA were taken as experimental group, and those cells treated with the control virus and without any treatment were taken as control group and blank group. Cell migration and cell aggression was examined by Tran-swell assay. Cells of the three groups were injected into nude mices subcutaneously with cell concentration of 1. 0 × 107/200 |xL respectively. The growth of tumor was examined for 7 weeks. Results The cell migration and aggression in experimental group were significantly suppressed compared with those in control group or blank group (all P <0.05) . The subcutaneous tumors in the experimental group occurred later and were smaller than those in control group or blank group ( all P < 0. 05 ) . Conclusion CD55 gene might play an important role in the regulation of cell migration, cell aggression and tumor formation in human pancreatic cancer cell line BxPC-3, and maybe used as a promising therapeutic target for pancreatic carcinoma.
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