Ectopic circSTK39 expression ameliorates hydrogen peroxide-induced human lens epithelial cell apoptosis and oxidative stress through the miR-125a-5p/ERCC6 pathway

unassigned: More and more studies suggest that circular RNA (circRNA) is involved in the pathogenesis of age-related cataract (ARC). CircSTK39, a circular RNA, has inhibitory effects on cancer progression. However, there is no data regarding the role of circSTK39 in ARC occurrence and the underlying mechanism. unassigned: ARC cell model was established by inducing lens epithelial cells (SRA01/04) using hydrogen peroxide (HO). CircSTK39, microRNA-125a-5p (miR-125a-5p) and ERCC excision repair 6, chromatin remodeling factor (ERCC6) expression were detected by quantitative real-time polymerase chain reaction. Western blot was conducted to assess protein expression. Cell viability, proliferation and apoptosis were investigated by cell counting kit-8 assay, 5-Ethynyl-29-deoxyuridine assay and flow cytometry analysis, respectively. Oxidative stress was evaluated using commercial kits. Dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay were used to identify the relationship between miR-125a-5p and circSTK39 or ERCC6. unassigned: CircSTK39 and ERCC6 expression were significantly downregulated, but miR-125a-5p expression was upregulated in the lens tissues of ARC patients and HO-treated SRA01/04 cells. HO treatment led to decreased cell proliferation and increased cell apoptosis and oxidative stress, accompanied by the increases of C-caspase3 and Bax expression and the decrease of Bcl-2 expression; however, these effects were reversed after circSTK39 overexpression. MiR-125a-5p was found to participate in HO-triggered cell damage by interacting with circSTK39. Additionally, ERCC6 silencing inhibited circSTK39 overexpression-mediated action. Importantly, circSTK39 regulated ERCC6 expression by interaction with miR-125a-5p in HO-treated SRA01/04 cells. unassigned: The increased expression of circSTK39 ameliorated HO-induced SRA01/04 cell injury through the miR-125a-5p/ERCC6 pathway.