miRNA‑124 regulates palmitic acid‑induced epithelial‑mesenchymal transition and cell migration in human retinal pigment epithelial cells by targeting LIN7C
- Xiao-Dong Han
- Xu-Guang Jiang
- Min Yang
- Wen-Jun Chen
- Li-Gang Li
Affiliations: Department of Ocular Fundus Diseases, Xi'an Aier Ancient City Eye Hospital, Xi'an, Shaanxi 710082, P.R. China, Department of Cataracts, Xi'an Aier Ancient City Eye Hospital, Xi'an, Shaanxi 710082, P.R. China
- Published online on: June 1, 2022 https://doi.org/10.3892/etm.2022.11408
Copyright: © Han
et al. This is an open access article distributed under the
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The present study revealed that palmitic acid (PA) treatment induced epithelial‑mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells, which are involved in the progression of proliferative vitreoretinopathy (PVR). ARPE‑19 cells were treated with PA followed by miRNA screening and EMT marker detection using qRT‑PCR. Then, miR‑124 mimic or inhibitor was transfected into ARPE‑19 cells to explore the role of miR‑124 on the EMT of ARPE‑19 cells using transwell assay. The underlying mechanism of miRNA were predicted by bioinformatics method and confirmed by luciferase activity reporter assay. Furthermore, gain‑of‑function strategy was also used to explore the role of LIN7C in the EMT of ARPE‑19 cells. The expression of miRNA or mRNA expression was determined by qRT‑PCR and the protein expression was determined using western blot assay. The result presented that PA reduced the expression of E‑cadherin/ZO‑1 whilst increasing the expression of fibronectin/α‑SMA. In addition, PA treatment enhanced the expression of microRNA (miR)‑124 in ARPE‑19 cells. Overexpression of miR‑124 enhanced PA‑induced upregulation of E‑cadherin and ZO‑1 expression and downregulation of fibronectin and α‑SMA. Moreover, miR‑124 mimic also enhanced the migration of ARPE‑19 cells induced by PA treatment. Inversely, miR‑124 inhibitor presented opposite effect on PA‑induced EMT and cell migration in ARPE‑19 cells. Luciferase activity reporter assay confirmed that Lin‑7 homolog C (LIN7C) was a direct target of miR‑124 in ARPE‑19 cells. Overexpression of LIN7C was found to suppress the migration ability and expression of fibronectin and α‑SMA, while increasing expression of E‑cadherin and ZO‑1; miR‑124 mimic abrogated the inhibitive effect of LIN7C on the EMT of ARPE‑19 cells and PA further enhanced this abolishment. Collectively, these findings suggest that miR‑124/LIN7C can modulate EMT and cell migration in RPE cells, which may have therapeutic implications in the management of PVR diseases.