MicroRNA-34a inhibits epithelial-mesenchymal transition of lens epithelial cells by targeting Notch1.

Posterior capsule opacification (PCO) is a common long-term complication of modern cataract surgery. The epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) is a crucial process in the development of PCO. The purpose of this study is to investigate the role of microRNA-34a (miR-34a) in the regulation of EMT and its target gene. Human LECs were treated with TGFβ2 to induce EMT as a model for PCO. The mRNA levels of miR-34a and EMT markers were examined by real-time quantitative polymerase chain reaction (qPCR). The expression level of miR-34a was downregulated, whereas that of Notch1 was upregulated in TGFβ2-induced EMT of LECs. Overexpression of miR-34a by transfection with miR-34a inhibited EMT of LECs and reduced the expression of Notch1; while, inhibition of miR-34a upregulated the expression of both Notch1 and its ligand Jagged1 in LECs. Luciferase reporter assays revealed that Notch1 gene was direct target of miR-34a. Moreover, DAPT, a specific inhibitor of Notch signaling pathway, reversed LEC-EMT. In addition, the expression level of miR-34a was downregulated, whereas that of Notch1 was upregulated in capsular opacification from cataract samples. MiR-34a can negatively regulate EMT of LECs by targeting Notch1. Therefore, miR-34a/Notch1 could serve as a potential therapeutic approach for the treatment of PCO.