LINC00963 silencing inhibits the proliferation and migration of high glucose‑induced retinal endothelial cells via targeting miR‑27b
- Rui Zhang
- Chunhong Niu
- Yuhan Guan
- Jianhua Wu
- Liping Hu
Affiliations: Fundus Disease Department, Aier Eye Hospital of Wuhan University, Wuhan, Hubei 430063, P.R. China, Department of Nursing, The Tianjin 4th Central Hospital, Tianjin 300140, P.R. China
- Published online on: September 8, 2021 https://doi.org/10.3892/etm.2021.10709
Copyright: © Zhang
et al. This is an open access article distributed under the
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The association between long intergenic non‑protein‑coding RNA 963 (LINC00963) and diabetes has not been fully elucidated. Therefore, the present study aimed to investigate the effect of the long non‑coding RNA LINC00963 on diabetic retinopathy (DR), in order to provide a new therapeutic target for this condition. Human retinal capillary endothelial cells (HRECs) were induced with high concentrations of glucose to establish a DR model. The expression levels of LINC00963, cell viability, the protein expression levels of proliferating cell nuclear antigen (PCNA) and Ki67, and the migratory capacity of HRECs were determined using reverse transcription‑quantitative PCR (RT‑qPCR), Cell Counting Kit‑8 assay, western blot analysis, and wound healing and Transwell assays, respectively. Furthermore, the Encyclopedia of RNA Interactomes database was used to predict the binding targets of LINC00963, and luciferase reporter assay was used to verify the direct binding of microRNA (miR)‑27b to LINC00963. RT‑qPCR was also utilized to measure the expression levels of miR‑27b, PCNA and Ki67. The results demonstrated that LINC00963 silencing inhibited glucose‑induced HREC proliferation and migration, and downregulated PCNA and Ki67 expression. Following transfection with miR‑27b inhibitor, cell proliferation and migration were notably enhanced, and the protein expression levels of PCNA and Ki67 were increased. Taken together, the results of the present study suggested that the LINC00963/miR‑27b axis may regulate the proliferation and migration of glucose‑induced HRECs. Therefore, LINC00963 may be considered as a potential therapeutic target for DR.