摘要
目的探讨上调叉头框转录因子M1(FoxM1)基因对人卵巢癌细胞迁移侵袭的影响及其分子机制。方法构建FoxM1过表达慢病毒载体。HO-8910细胞分为3组,空白对照组、空载对照组和FoxM1慢病毒过表达组。转染HO-8910细胞后,采用Westernblot方法观察FoxM1蛋白表达,采用划痕修复试验检测癌细胞迁移能力,采用Transwell方法检测癌细胞侵袭能力,采用Westernblot法检测癌细胞E-钙黏蛋白和N-钙黏蛋白水平。结果与空白对照组和空载对照组比较,FoxM1过表达组FoxM1蛋白明显升高。划痕修复试验结果显示,空白对照组、空载对照组和FoxM1过表达迁移细胞迁移距离分别为(156.80±2.26)、(161,60±1.81)和(278.60±2.62)μm。统计学分析发现,与空白对照组比较,P〈0.01;Transwell侵袭试验显示,空白对照组、空载对照组和FoxM1过表达迁移细胞数分别为(68.56±1.69)、(67.27±1.36)和(126.38±1.56)个。统计学分析发现,与空白对照组比较,P〈0.01。Westernblot结果显示,与空白对照组比较,FoxM1过表达细胞组E-钙黏蛋白表达降低,而N-钙黏蛋白表达增高。结论FoxM1过表达可促进人卵巢癌细胞迁移和侵袭能力,其机制可能与促进上皮一间充质转化有关。
Objective To explore the effects and mechanism of over- expression of Forkhead box protein M1 (FoxM1) gene on the migration, and invasion and epithelial -mesenchymal transition (EMT) of human ovarian cancer cells. Methods FoxM1 over - expression of the virus vector was constructed. All HO- 8910 cells were divided into three groups, the control group (Con- A), Lentiviral vector(LV) con- trol group (Con - B) and over - expression group FoxM1. After three group HO -8910 cells was transfect- ed with phosphate buffer (PBS), Lentiviral vector (LV), and LV -FoxM1, the protein levels of FoxM1 were determined by Western blotting, respectively. The migration and invasion ability was evaluated by wound healing assay and Transwell assay, respectively. The E - Cadherin and N - Cadherin of protein of cancer ceils was examined by Western blotting assay. Results The results from Western blotting assay showed that the levels protein of FoxM1 were greatly increased in HO - 8910 cancer cells transfected with LV- FoxM1. The results of the wound healing test showed that the migration distance of Con - A, Con - B, and LV - FoxM1 group was( 156. 80 ±2. 26), ( 161.60 ± 1.81 ) and (278.60 ± 2. 62) μm, respectively (P 〈0. 01 ) ; The results of the Transwell invasion assay showed that the membrane cell number of Con - A, Con - B, and LV - FoxM1 group was (68. 56 ± 1.69) and (67.27 ± 1.36) and ( 126. 38 ± 1.56), respectively (P 〈0. 01 ); Compared with the Con -A, there were E -cadherin protein expression de- creased ; however, N - cadherin protein increased in HO - 8910 cancer cells transfected with LV - FoxM1. Conclusion FoxM1 overexpression can promote human ovarian cancer cell migration and invasion, and its mechanism may be related to the promotion of epithelial - mesenchymal transition.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2016年第12期2748-2751,共4页
Chinese Journal of Experimental Surgery
基金
江苏省省级重点研发专项基金(BE2015666)
镇江市社会发展基金(SH2013044、SH2015050、SH2015061)
关键词
卵巢肿瘤
叉头框转录因子1
迁移
侵袭
上皮一间充质转化
Ovarian carcinoma
Forkhead box protein MI
Migration
Invasion
Epitheli al - mesenchymal transition