Purpose: Cataract is a leading visual disease characterized by enhanced oxidative stress and increased apoptosis of human lens epithelial cells (HLECs). TRIM3 is a tumor suppressor in many cancers. However, its role in cataract remains unknown. In this study, we aimed to explore the role of TRIM3 in HO-injured HLECs and the underlying mechanisms involved.
Methods: HLECs were treated with different HO concentrations to induce apoptosis. A lentivirus was designed to overexpress TRIM3 and p53, and TRIM3 knockdown was prepared. A P53 inhibitor, PFTα, was used to knockdown p53. Cell viability and apoptosis were detected by CCK-8 and flow cytometric analyses, respectively. TRIM3, p53, Bcl2, and Bax expression levels were determined by qRT-qPCR and western blotting.
Results: It was found that HO-treated HLECs had markedly decreased cell viability and TRIM3 expression. TRIM3 overexpression attenuated the HO-induced HLEC apoptosis, while TRIM3 knockdown promoted it. P53, a downstream target of TRIM3, was found to be negatively regulated by TRIM3 via ubiquitination in HLECs. Furthermore, p53 overexpression abolished the effect of TRIM3 overexpression on HO-induced HLEC apoptosis, while PFTα alleviated the TRIM3 knockdown-mediated HLEC apoptosis.
Conclusion: This study demonstrates that TRIM3 inhibited the HO-induced apoptosis of HLECs by decreasing p53 via ubiquitination.
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