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Regulation of long-chain non-coding RNA01592 (LINC01592) in the process of transforming retinal pigment epithelial (RPE) cells into mesenchymal cells following induction by transforming growth factor beat 1 (TGF-β1) was investigated by interfering with LINC01592 expression in human RPE (hRPE) cells. LINC01592 expression in hRPE cells was significantly increased following treatment with 10 ng/mL TGF-β1 for 48 h. Expression of E-cadherin and Snail were decreased in hRPE cells following induction with TGF-β1 compared with the control group ( P &lt; 0.05). Following induction by TGF-β1, expression of E-cadherin, alpha-smooth muscle actin (α-SMA), and Snail were significantly lower in the LINC01592-knockdown group compared with the negative control group ( P &lt; 0.05). LINC01592 overexpression significantly enhanced the viability, proliferation, and migration of hRPE cells induced by TGF-β1 ( P &lt; 0.05). Following induction by TGF-β1, E-cadherin expression was significantly decreased and α-SMA and Snail expression were significantly increased in the LINC01592-overexpression group compared with the negative control group ( P &lt; 0.05). RPE cells induced by TGF-β1 exhibited epithelial-mesenchymal transition (EMT). Inhibiting LINC01592 expression could significantly reduce TGF-β1-induced EMT of hRPE cells. The regulatory effect of LINC01592 on EMT in hRPE cells induced by TGF-β1 provides a novel treatment for proliferative vitreoretinopathy.

Role of LINC01592 in TGF-β1-induced epithelial-mesenchymal transition of retinal pigment epithelial cells