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

作者：Wang, Chao; Zhao, Baowen; Fang, Jiahui; Shi, Zhan^*

来源：Contrast Media & Molecular Imaging, 2022, 2022: 5383146.

DOI：10.1155/2022/5383146

• GROWTH-FACTOR-I
• CATARACT-SURGERY
• INSULIN
• OPACIFICATION
• FIBROSIS
• EMT

The abnormal proliferation, migration, and epithelial-mesenchymal transformation (EMT) of lens epithelial cells (LECs) are the main reasons for 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 cataracts, 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-beta 2-induced EMT of LECs. Additionally, to evaluate valuable microRNAs (miRNAs) which target IGF-1 to modulate LEC-EMT, we predicted miR-3666 might regulate IGF-1 by binding its 3'UTR according to the bioinformatics database. Furthermore, we verified that miR-3666 directly targeted IGF-1 by luciferase reporter assay. By using miR-3666 mimics, cell proliferation, migration, and invasion were suppressed, while being enhanced by the reduction of miR-3666. Knockout of IGF1 reverses the effect of the miR-3666 inhibitor on the malignant behavior of LECs. These results indicate the role of miR-3666/IGF-1 in LEC-EMT that offers new strategies for the therapy and prevention of PCO.

• 单位
  哈尔滨医科大学; 1