As one of the first discovered lncRNAs, TUG1 has been reported to be widely expressed in a variety of tumours. It promotes cell proliferation, differentiation, apoptosis and migration. However, our understanding of its importance in cataracts is limited. This study aims to explore the mechanism by which TUG1 mediates the apoptosis of lens epithelial cells by regulating the miR-29b/Smac axis in age-related cataracts and to identify more strategies for the nonsurgical treatment of cataracts. In this experiment we found TUG1 and Smac were expressed at high levels in age-related cataract (ARC) samples and HLEB3 cells treated with H2O2, while miR-29b expression was decreased. In vitro cell-based experiments confirmed that the downregulation of TUG1 inhibits lens epithelial cell apoptosis. Mechanistically, Smac expression is negatively regulated by miR-29b. TUG1 competitively inhibits miR-29b expression and causes the release of more Smac. In addition, miR-29b reverses the effect of TUG1 on HLE-B3 cells. In conclusion, lncRNATUG1 increases Smac expression by competitively inhibiting miR-29b and promoting the apoptosis of lens epithelial cells in age-related cataracts. This mechanism is the cytological basis of ARC formation. Based on these results, the TUG1-miR29b-Smac axis may be a new molecular pathway to regulate the development of age-related cataracts.

As one of the first discovered lncRNAs, TUG1 has been reported to be widely expressed in a variety of tumours. It promotes cell proliferation, differentiation, apoptosis and migration. However, our understanding of its importance in cataracts is limited. This study aims to explore the mechanism by which TUG1 mediates the apoptosis of lens epithelial cells by regulating the miR-29b/Smac axis in age-related cataracts and to identify more strategies for the nonsurgical treatment of cataracts. In this experiment we found TUG1 and Smac were expressed at high levels in age-related cataract (ARC) samples and HLEB3 cells treated with H2O2, while miR-29b expression was decreased. In vitro cell-based experiments confirmed that the downregulation of TUG1 inhibits lens epithelial cell apoptosis. Mechanistically, Smac expression is negatively regulated by miR-29b. TUG1 competitively inhibits miR-29b expression and causes the release of more Smac. In addition, miR-29b reverses the effect of TUG1 on HLE-B3 cells. In conclusion, lncRNATUG1 increases Smac expression by competitively inhibiting miR-29b and promoting the apoptosis of lens epithelial cells in age-related cataracts. This mechanism is the cytological basis of ARC formation. Based on these results, the TUG1-miR29b-Smac axis may be a new molecular pathway to regulate the development of age-related cataracts.