Effects of miR-153-3p on glioma cell invasion, migration and epithelial mesenchymal transformation via targeting TGFβ2 / 西安交通大学学报(医学版)

ABSTRACT

Objective: To investigate the targeting relationship between microRNA-153-3p and transforming growth factor-beta 2 (TGFβ2) and its effects on invasion, migration and epithelial-mesenchymal transformation of cultured glioma cells. Methods: Real-time fluorescence quantitative PCR and Western blotting were used to detect the effects of miR-153-3p on the expressions of TGFβ2 mRNA and protein. Bioinformatics software was used to predict the binding sites of miR-153-3p to TGFβ2. Luciferase reporter assay was used to analyze the targeting relationship between miR-153-3p and TGFβ2. Transwell and wound healing assays were used to detect the effects of miR-153-3p on SHG-44 cells invasion and migration. Western blotting was used to detect the expressions of proteins related to invasion, migration and epithelial-mesenchymal transition. Results: miR-153-3p mimic inhibited the expressions of TGFβ2 mRNA and protein in SHG-44 cells. Software predicted results showed a continuous binding region between miR-153-3p and TGFβ2. miR-153-3p mimic co-transfected with TGFβ2 wild-type reporter vector significantly decreased the activity of luciferase in the cells (P<0.01). miR-153-3p mimic co-transfected with TGFβ2 mutant reporter showed no significant change in luciferase activity. The number of invasive cells and scratch closure rate of SHG-44 cells transfected with miR-153-3p mimic were significantly decreased. The expression levels of MMP-2, MMP-9 and VEGF were significantly decreased. The expression levels of N-cadherin, Snail-2, Vimentin and Twist were significantly decreased, and the expression level of E-cadherin was significantly increased (P<0.01). The high expression of TGFβ2 alleviated the effect of miR-153-3p on the cell invasion and epithelial mesenchymal transition related proteins in SHG-44. Conclusion: miR-153-3p inhibits the invasion and migration of cultured glioma cells and epithelial mesenchymal transition by targeting TGFβ2.