CircRNA HLCS regulates lens epithelial cell apoptosis via miR-338-3p/BPNT1 axis

• Published in: International ophthalmology 2024-03, Vol.44 (1), p.142-142, Article 142
• Main Authors: Sun, Lianyi, Li, Fengzhi, Bai, Shuwei, Bi, Chunchao
• Format: Article
• Language: English
• Subjects: Age; Antibodies; Apoptosis; Cataracts; Cell proliferation; Cell viability; Cells; Circular RNA; Epithelial cells; Epithelium; Flow cytometry; Hospitals; Medicine; Medicine & Public Health; MicroRNAs; miRNA; Nucleotidase; Ophthalmology; Original Paper; Polymerase chain reaction; Ribonucleic acid; RNA; Therapeutic targets
• ISSN: 1573-2630; 0165-5701; 1573-2630
• DOI: 10.1007/s10792-024-03082-0

Purpose The purpose of this study was to investigate the effect of circ_HLCS on age-related cataract (ARC). Methods Circ_HLCS, microRNA (miR)-338-3p, and bisphosphate 3′-nucleotidase 1 (BPNT1) were quantified by quantitative real-time polymerase chain reaction or western blot. Cell proliferation and cell viability were assessed by the 5-Ethynyl-2′-deoxyuridinr and cell counting kit-8 assays. Cell apoptosis was detected by flow cytometry. Targeted correlations among circ_HLCS, miR-338-3p, and BPNT1 were verified by the dual-luciferase reporter and RNA pull-down assays. Results circ_HLCS was diminished in ARC tissues and UV-treated SRA01/04 cells. Elevated content of circ_HLCS undermined UV-induced cell proliferation inhibition and apoptosis. Mechanistically, circ_HLCS directly targeted miR-338-3p, and circ_HLCS regulated BPNT1 expression through miR-338-3p. Furthermore, reduction of miR-338-3p ameliorated UV-induced SRA01/04 cell damage by increasing BPNT1 expression. Conclusion Taken together, these data suggested that circ_HLCS inhibited apoptosis of UV-treated SRA01/04 cells by miR-338-3p/BPNT1 axis. Therefore, circ_HLCS might be a potential therapeutic target for ARC.