TRIM3 Inhibits H₂O₂-Induced Apoptosis in Human Lens Epithelial Cells by Decreasing p53 via Ubiquitination

Abstract

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 H₂O₂-injured HLECs and the underlying mechanisms involved.

Methods

HLECs were treated with different H₂O₂ 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 H₂O₂-treated HLECs had markedly decreased cell viability and TRIM3 expression. TRIM3 overexpression attenuated the H₂O₂-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 H₂O₂-induced HLEC apoptosis, while PFTα alleviated the TRIM3 knockdown-mediated HLEC apoptosis.

Conclusion

This study demonstrates that TRIM3 inhibited the H₂O₂-induced apoptosis of HLECs by decreasing p53 via ubiquitination.

Keywords:

• Apoptosis
• human lens epithelial cells
• p53
• TRIM3
• ubiquitination

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The data that support the findings of this study are available from the corresponding author CW upon reasonable request.