Molecular mechanism of non-coding RNA targeting zinc finger binding protein 1 and cervical cancer cells suppression

Abstract

The main aim of the study is to explore the mechanism of microrNA-145-3p targeting ZEB1 on migration and invasion in cervical cancer cells. In this study, cervical cancer cell line C33A was selected and transfected. After transfection of C33A cells, the expression level of Mir-145-3p was measured by QT-PCR. Human cervical cancer cell line (C33A) was cultured in RPMI 1640 medium and cell transfection experiment was performed. The related targets of Mir-145-3p, and a complementary binding site was found between the 3′UTR terminal of ZEB1 and Mir-145-3p was performed using a Targetscan biological software. The luciferase reporter system was used to determine the targeting relationship between Mir-145-3p and complementary binding site. The expression of e-cadherin and vimentin proteins was detected by western blot analysis. After 48 h, the expression level of Mir-145-3p in mimics group was significantly increased, the inhibitor group was significantly down-regulated and was statistically significant (P < 0.05). The clone formation, migration and invasion ability and vimentin expression in the MIMics group were significantly decreased than NC group. However, the apoptosis rate and e-cadherin protein expression were significantly increased than control group. In the inhibitor group, the cell cloning, cell migration, invasion and vimentin protein expression were significantly increased, while the cell apoptosis rate and e-cadherin protein expression were significantly decreased (P < 0.05). Analysis of luciferase expression genes revealed that mirNa-145-3p and ZEB1 have targeted regulatory relationship. Compared with Mir-NC, there was no significant difference between Mir-145-3p MUT and Mir-NC (P > 0.05), and luciferase activity of Mir-145-3p WT was significantly down-regulated (P > 0.05). Overexpression of microrNA-145-3p downregulated ZEB1 expression and inhibited proliferation, migration, invasion, and epithelial-mesenchymal transformation of cervical cancer cells, and promoted cell apoptosis.