miR-100对食管鳞癌细胞株Ec-109的抑制作用

Tumor Suppressor Roles of mi R-100 in Esophageal Squamous Cell Carcinoma Cell Line Ec-109

目的探讨mi R-100对食管鳞癌细胞的调控作用。方法构建携带GFP的mi R-100表达质粒,脂质体转染食管鳞癌细胞株Ec-109。分别利用流式细胞仪、细胞划痕和Transwell实验检测mi R-100对细胞周期、凋亡和迁移的调节作用。结果在食管鳞癌细胞中高表达mi R-100可诱导G1期阻滞,即停留于G1期的细胞数量增加,进入S和G2/M期的数量减少;在无血清培养的条件下mi R-100的高表达可促进细胞凋亡同时抑制食管鳞癌细胞迁移。结论 mi R-100在食管鳞癌细胞株Ec-109中高表达可诱导细胞周期G1期阻滞、抑制细胞的迁移并促进其凋亡。

Objective To investigate the biological functions of mi R-100 in esophageal squamous cell carcinoma(ESCC) cell. Methods mi R-100 was cloned into a GFP expressing vector, which was further transfected into esophageal squamous cell carcinoma cell line Ec-109 by Lilpofectamine, and GFP positive cells were then selected by flow cytometry. Cell cycle, apoptosis and migration were analyzed by flow cytometry, wound healing and Transwell assay, respectively, upon the expression of mi R-100 in Ec-109 cells. Results The high expression of mi R-100 could induce G1 arrest: the percentage of cells number were increased in the G1 phase, while cells in the S or G2/M were decreased. Under the serum free culture condition, the presence of mi R-100 could enhance cell apoptosis and also suppress Ec-109 cells migration. Conclusion The exogenous expression of mi R-100 exhibits a tumor suppressor role in esophageal squamous cell carcinoma cell line Ec-109, including inducing G1 arrest, suppressing cell migration and promoting cell apoptosis.