中文摘要：

用前期设计并合成好的重组腺病毒质粒pAdsiALK2,经Pac I酶切后转染至HEK293细胞进行包装,制备重组腺病毒,扩增后进行病毒滴度测定,以重组腺病毒siALK2（AdsiALK2）感染MDA-MB-231细胞,以含RFP的腺病毒作为感染对照,并设空白对照组。通过RT-PCR验证MDA-MB-231细胞中ALK2表达显著下降;MTT法、平板集落形成试验、细胞划痕试验及Transwell侵袭试验证实MDA-MB-231/siALK2组相比MDA-MB-231/RFP组细胞的增殖活力、集落形成率及划痕愈合率均显著降低（P〈0.05）,穿膜细胞数也明显减少（P〈0.05）,而MDA-MB-231/RFP组与空白对照组比较,差异无统计学意义（P〉0.05）。该研究表明,下调ALK2表达后可以在体外抑制乳腺癌MDA-MB-231细胞的增殖、迁移与侵袭。

英文摘要：

The recombinant adenovirus plasmid pAdsiALK2 was digested with Pac I and transfected to HEK293 packaging cells. The recombinant adenovirus was amplified and identificated, MDA-MB-231 cells were infected with adenovirus siALK2 and RFP respectively. RT-PCR demonstrated that ALK2 expression was remarkably decreased in MDA-MB-231/siALK2 cells. The proliferation, migration and invasion of MDA-MB-231/siALK2 cells were estimated by MTT assay, colony-forming assay, wounding healing assay and transwell assay showed that the pro- liferation activity, colony formation rate, wound healing rate and count of cells crossing the matrix barrier were signifi- cantly reduced in MDA-MB-231/siALK2 group than those in MDA-MB-231/RFP group （P〈0.05）, ALK2 expression was remarkably decreased in MDA-MB-231/siALK2 cells. But no significant difference was observed between MDA- MB-231/RFP and blank control groups （P〉0.05）. These results demonstrated that down-regulating ALK2 expressioncan inhibite the proliferation, migration and invasion ofMDA-MB-231 cells in vitro.