lncRNA MIAT increases cell viability, migration, EMT and ECM production in age‑related cataracts by regulating the miR‑181a/CTGF/ERK signaling pathway
- Jiaojiao Ling
- Ke Tan
- Lu Lu
- Fang Yang
- Lan Luan
Affiliations: Department of Ophthalmology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, P.R. China
- Published online on: May 13, 2020 https://doi.org/10.3892/etm.2020.8749
Copyright: © Ling
et al. This is an open access article distributed under the
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Age-related cataract (ARC) is a common cause of blindness in elderly individuals. Long non‑coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) has been reported to participate in various biological processes in a number of diseases; however, the biological mechanism underlying MIAT during ARC is not completely understood. The expression levels of MIAT, microRNA (miR)‑181a and connective tissue growth factor (CTGF) were measured by reverse transcription‑quantitative PCR. The protein expression levels of CTGF, α‑smooth muscle actin, fibronectin, collagen type I, ERK, phosphorylated (p)‑ERK, mitogen‑activated protein kinase (MEK), and p‑MEK were detected by western blotting. Cell viability and migration were assessed using MTT and Transwell assays, respectively. Moreover, a dual‑luciferase reporter assay was performed to investigate the interaction between miR‑181a and MIAT or CTGF. MIAT and CTGF were upregulated, while miR‑181a was significantly downregulated in ARC tissues compared with normal tissues. MIAT or CTGF knockdown decreased cell viability, migration, epithelial‑mesenchymal transition and extracellular matrix production in TGF‑β2‑treated SRA01/04 cells. It was hypothesized that miR‑181a may be sponged by MIAT and may target CTGF. Furthermore, the miR‑181a inhibitor reversed the inhibitory effect of MIAT knockdown on the progression of TGF‑β2‑treated SRA01/04 cells. Moreover, CTGF knockdown also reversed MIAT overexpression‑mediated progression of TGF‑β2‑treated SRA01/04 cells. In addition, MIAT and CTGF regulated the activity of the ERK signaling pathway. The results suggested that MIAT may regulate the progression of ARC via the miR‑181a/CTGF/ERK signaling pathway, which may serve as a novel therapeutic target for ARC.