miR-128, ZEB1 对子宫内膜癌细胞迁移侵袭 和上皮间质转化的影响及其靶向关系验证.

Objective To observe the effects of miR-128 and ZEB1 on the migration, invasion and epithelial mesen‐ chymal transition( EMT) of endometrial carcinoma( EC) cells and to verify the targeted relationship between them. Meth⁃ ods The qRT-PCR and Western blotting were used to detect the relative expression levels of miR-128 and ZEB1 in three EC cell lines( HEC-1A, Ishikawa, and KLE) and one endometrial epithelial cell line hEEC, respectively. Ishikawa cell line with the lowest expression level of miR-128 was taken as the follow-up study object. Ishikawa cells were divided into the negative control group and miR-128 overexpression group, and were transfected with miRNA-NC and miR-128 mim‐ ics, respectively. After 48 h, the cells were collected for follow-up experiments. Cell Scratch test and Transwell test were used to detect the migration and invasion abilities of cells in each group after transfection. Western blotting was used to de‐ tect ZEB1, E-cadherin, Fibronectin and Vimentin protein of cells in each group after transfection. Double luciferase re‐ porter gene experiment was used to verify the targeted regulatory relationship between miR-128 and ZEB1. Results Com‐ pared with hEEC, the expression of miR-128 in EC cell lines HEC-1A, Ishikawa and KLE decreased( all P<0. 05), and the expression of ZEB1 protein increased( P<0. 05) . After transfection, the expression of miR-128 increased significantly in Ishikawa cells( P<0. 05), the number of transmembrane cells and scratch healing rate decreased( all P<0. 05), the rel‐ ative expression levels of ZEB1, Fibronectin and Vimentin decreased( all P<0. 05), and the expression of E-cadherin protein increased( P<0. 05). The results of double luciferase reporter gene experiment showed that miR-128 could target and regulate ZEB1 gene( P<0. 05). Conclusions MiR-128 can inhibit the migration, invasion and EMT of Ishikawa cells. ZEB1 can promote the migration, invasion and EMT of Ishikawa cells. MiR-128 and ZEB1 have a targeted regulatory rela‐ tionship. [ABSTRACT FROM AUTHOR]