摘要
目的研究mi R-186靶向PIG11基因抑制胃癌细胞的侵袭。方法首先通过生物信息学方法分析,寻找与PIG11(TP53I11)结合的靶mi RNAs。分别构建mi R-186 mimics、点突变序列(Point mutation,PM)、空白载体(Scramble),转染胃癌MKN-28细胞。q RT-PCR检测mi R-186表达,Western blot检测PIG11表达,分析mi R-186表达和PIG11表达之间的相关性。Transwell检测转染前后各组胃癌MKN-28细胞侵袭能力变化。结果生物信息学发现12个mi RNAs可能是PIG11的潜在靶mi RNAs,其中mi R-186与PIG11结合特异性最好、稳定性最强;MKN-28-mi R-186 mimics细胞株中mi R-186表达增高,而PIG11表达下调,而MKN-28、MKN-28-mi R-Scramble、MKN-28-mi R-186-PM 3个细胞株中mi R-186表达水平较低,而PIG11表达水平较高。MKN-28-mi R-186 mimics侵袭细胞计数明显低于其他3组(P<0.05)。结论 mi R-186有可能靶向结合PIG11,下调其表达并抑制胃癌细胞的侵袭。
Objective To study the mechanism of miR-186 targeted to PIG11 and inhibit metastasis and invasion of gastric cancer cells. Methods Bioinformatics were used to analyze the miRNAs targeted to PIG11. qRT-PCR detected the level of miR-186 in gastric cancer cell lines MKN-28. The expression of PIG11 were detected by Western blot. And the changes of ability of metastasis and invasion were examined by Transwell. Results There were high expression of miR-186 and low expression of PIG11 in MKN-28-miR-186 mimics. There were low expression of miR-186 and high expression of PIG11 in MKN-28, MKN-28-miR-Scramble, MKN-28-miR-186-PM（P〈0.05）. There were smaller invaded cells in MKN-28-miR-186 mimics than in other three cell lines （P〈0.05）. Conclusion miR-186 can target to PIG11 and down regulate its expression and inhibit metastasis and invasion of gastric cancer cells.
出处
《中国现代医药杂志》
2015年第1期1-4,共4页
Modern Medicine Journal of China
基金
湖南省普通高等学校科学研究项目(编号:11C1091)
