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  • Title: miRNA-181a inhibits the proliferation, migration, and epithelial-mesenchymal transition of lens epithelial cells.
    Author: Dong N, Tang X, Xu B.
    Journal: Invest Ophthalmol Vis Sci; 2015 Jan 27; 56(2):993-1001. PubMed ID: 25626972.
    Abstract:
    PURPOSE: 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). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
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