TUG1 promotes lens epithelial cell apoptosis by regulating miR-421/caspase-3 axis in age-related cataract

Background: Age-related cataract is among the most common chronic disorders of ageing and the apoptosis of lens epithelial cells contributes to non-congenital cataract development. We amid to explore the role of TUG1 and miR-421 in the age-related cataract. Methods: The expression level of TUG1, miR-421 and caspase-3 were detected by RT-qPCR. The apoptoticrelated protein, caspase-3, Bax and blc-2 were analyzed by western blot. We performed ultraviolet (UV) irradiation to induce SAR01/04 cell apoptosis which was analyzed by flow cytometry. RIP pull-down and luciferase reporter assay were used to verified the combination and regulating among TUG1, miR-421 and caspase-3. Results: Here, we observed that the expression level of TUG1 and caspase-3 in the anterior lens capsules of age related cataract were significantly higher and miR-421 was significantly lower than that in the normal anterior lens capsules. The apoptosis-related protein, caspase-3, Bax and blc-2 were abnormal expression in the anterior lens capsules of age-related cataract tissue. Our data showed that the expression level of TUG? and caspase-3 and cell apoptosis rate in SARO1/04 cells treated with UV irradiation was remarkably higher than that in the control. TUG? negatively regulated miR-421 expression and promoted UV irradiation-induced SARO1/04 cell apoptosis. However, miR-421 inhibitor and pcDNA-caspase-3 could reverse the action of the SRA01/04 cell apoptosis by si-TUG1, which suggested TUG1 promoted UV irradiation-induced apoptosis through down regulating miR-421 expression. Furthermore, this study confirmed TUG1 could been in combination with miR421, and TUG1 and caspase-3 were both a directly target of miR-421, Conclusion: TUG1 modulated lens epithelial cell apoptosis through miR-421/caspase-3 axis. These findings will offer a novel insight into the pathogenesis of cataract.