miRNA-181a inhibits the proliferation, migration, and epithelial-mesenchymal transition of lens epithelial cells

• Published in: Investigative ophthalmology & visual science Vol. 56; no. 2; pp. 993 - 1001
• Main Authors: Dong, Ning, Tang, Xin, Xu, Bing
• Format: Journal Article
• Language: English
• Published: United States 27.01.2015
• Subjects: Adult; Aged; Aged, 80 and over; Blotting, Western; Capsule Opacification - genetics; Capsule Opacification - metabolism; Capsule Opacification - pathology; Cell Movement; Cell Proliferation; Cells, Cultured; Epithelial Cells - metabolism; Epithelial Cells - pathology; Epithelial-Mesenchymal Transition - genetics; Female; Gene Expression Regulation; Humans; Lens, Crystalline - metabolism; Lens, Crystalline - pathology; Male; MicroRNAs - biosynthesis; MicroRNAs - genetics; Middle Aged; Real-Time Polymerase Chain Reaction; RNA - genetics; Signal Transduction; migration; epithelial–mesenchymal transition; miR-181a; proliferation; lens epithelial cells
• ISSN: 0146-0404; 1552-5783
• DOI: 10.1167/iovs.14-15860

MicroRNA-181a (miR-181a) is thought to be involved in posterior capsule opacification (PCO). This study investigated the role of miR-181a in the proliferation, migration, and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). The expression of miR-181a was detected in human PCO-attached LECs and LECs obtained from patients with anterior polar cataracts by quantitative RT-PCR (qRT-PCR). The proliferation of SRA01/04 cells transfected with miR-181a mimics was analyzed by MTT assays and bromodeoxyuridine (BrdU)-incorporation assays. The migration of SRA01/04 cells was evaluated by wound-healing assays and Transwell migration. Luciferase reporter assays were used to validate the regulation of a putative target of miR-181a. The expression of miR-181a is decreased in human PCO-attached LECs and LECs obtained from patients with anterior polar cataracts. A significant decrease in proliferation was observed in SRA01/04 cells transfected with miR-181a mimics. The overexpression of miR-181a inhibited the migration ability of LECs. Downregulation of fibronectin, Slug, and cyclooxygenase-2 (COX-2) expression and upregulation of E-cadherin expression were induced in human PCO-attached LECs transfected with miR-181a mimics and miR-181a-overexpressing LECs obtained from patients with anterior polar cataracts. Furthermore, luciferase assays using a reporter carrying a putative miR-181a target site in the 3' untranslated region of c-Met, Slug, and COX-2 revealed that miR-181a directly targets c-Met, Slug, and COX-2. These data reveal that miR-181a can inhibit the proliferation, migration, and EMT of LECs and suggest that the restoration of miRNA-181a expression may be a potential novel therapeutic target for the prevention and treatment of posterior capsule opacification.