IGF-1 Promotes Epithelial-Mesenchymal Transition of Lens Epithelial Cells That is Conferred by miR-3666 Loss

Abstract The abnormal proliferation, migration and epithelial-mesenchymal transformation (EMT) of lens epithelial cells (LECs) are the main reasons of vision loss caused by posterior capsular opacification (PCO) after cataract surgery. Insulin-like growth factor-1 (IGF-1) was found to be associated with the pathogenesis of cataract, but its biological role in PCO is poorly understood. In the present study, IGF-1 overexpression facilitated the proliferation, migration and EMT, whereas knockdown of IGF-1 markedly suppressed the proliferation, migration and TGF-β2-induced EMT of LECs. Additionally, To evaluate valuable microRNAs (miRNAs) which target IGF-1 to modulate LECs-EMT, we predicted miR-3666 might regulate IGF-1 by binding its 3’UTR according bioinformatics database. Furthermore, we verified that miR-3666 directly targeted to IGF-1 by luciferase reporter assay. By using miR-3666 mimics, cells proliferation, migration, and invasion were suppressed, while were enhanced by reduction of miR-3666. Knockout of IGF1 reverses the effect of miR-3666 inhibitor on the malignant behavior of LECs. These results indicate the role for miR-3666/IGF-1 in LECs-EMT that offer new strategies for the therapy and prevention of PCO.