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Ning Dong, Xin Tang, Bing Xu; miRNA-181a Inhibits the Proliferation, Migration, and Epithelial–Mesenchymal Transition of Lens Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2015;56(2):993-1001. doi: https://doi.org/10.1167/iovs.14-15860.
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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.
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