miR-223在结肠癌组织中的表达及促进结肠癌细胞迁移侵袭的机制研究.

Objective: To investigate the expression of microRNA-223(mi R-223) in colon cancer and its influence and mechanism on the invasion and migration of HT-29 cells. Methods: The expression of mi R-223 in colon cancer and adjacent tissues was detected.mi R-223 mimics(mi R-223 mimics, mi R-223 mimics group) and microRNA unrelated sequences(mi R-223 NC, NC group) were transfected into colon cancer HT-29 cells by liposome transfection.Detection of mi R-223 and TWIST expression in transfected cells by Realtime PCR, Western blot was used to detect the protein expression of TWIST, and Tranwell was used to detect the cell migration and invasion. Double luciferase reporter gene was used to detect the effect of mi R-223 on the promoter activity of TWIST gene. Transwell migration and invasion assay was used to detect the migration and invasion of human colon cancer cell line HT-29 transfected with mi R-223 mimics and TWIST si RNA. Results: The expression of mi R-223 was significantly higher than that of the adjacent colon(P<0.05). Compared with the blank control group and mi R-223 NC group, the expression of mi R-223 in HT-29 cells transfected with mi R-223 mimics increased significantly(P<0.05). Compared with the negative control group and the empty transfection group, the number of cells penetrated by mi R-223 mimics transfection group increased significantly(P<0.05), and the cell invasion ability of mi R-223 mimics transfection group increased significantly(P<0.05). Compared with mi R-223 NC group and blank control group, the expression of TWIST gene m RNA and protein in HT-29 cells transfected with mi R-223 mimics increased significantly(P<0.05). Double luciferase analysis showed that TWIST was the downstream target gene of mi R-223. The migration and invasion ability of HT-29 cells co transfected with TWIST si RNA and mi R-223 mimics was significantly weaker than that of HT-29 cells alone transfected with mi R-223 mimics(P<0.05). Conclusions: mi R-223 may promote the migration and invasion of HT-29 cells by up regulating the level of downstream target gene TWIST. [ABSTRACT FROM AUTHOR]