LAUSR

Cataract, opacification of the lens, is one of the most important reasons of visual impairment and blindness. Though microRNAs (miRNAs) have been demonstrated to play important roles in cataractogenesis, the underlying molecular mechanisms in this progress remain obscure. In the present study, microRNA-23b-3p (miR-23b) overexpression promoted the proliferation, migration and epithelial-mesenchymal transition (EMT), whereas miR-23b knockdown markedly inhibited the proliferation, migration and TGF-β-induced EMT of lens epithelial cells (LECs). In TGF-β-induced LECs, the expression of miR-23b was markedly upregulated and the expression of Sprouty2 (SPRY2) was markedly downregulated, furthermore the mRNA and protein levels of SPRY2 were markedly decreased in miR-23b inhibitor-transfected LECs. We then performed a Dual-luciferase reporter assay to confirm that miR-23b directly targeted SPRY2. The promoted migration and EMT of LECs by enforced expression of miR-23b were suppressed by SPRY2 overexpression. The findings present the first evidence indicating that miR-23b can promote the proliferation, migration, and EMT of LECs by targeting SPRY2 and the inhibition of miR-23b may possess the therapeutic potential for cataract.