METTL3 mediates CPB1 expression by regulating transcription factor BACH2 to promote apoptosis and oxidative stress of lens epithelial cells.

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Tác giả: Yihui Bao, Yu Pan, Liqin Shao, Zhangxing Sheng

Ngôn ngữ: eng

Ký hiệu phân loại: 070.48346 Journalism

Thông tin xuất bản: United States : Journal of bioenergetics and biomembranes , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 248185

BACKGROUND: Cataracts are a significant cause of vision loss, adversely affecting the quality of human life. Numerous studies have reported that lens epithelial cells (LECs) play a crucial role in age-related cataract (ARC). However, the roles of carboxypeptidase B 1 (CPB1) and transcription factor BTB and CNC homologue 2 (BACH2) in the pathogenesis of ARC remain unclear. In this study, we aim to explore the contributions of CPB1 and BACH2 to the development of ARC. METHODS: The Gene Expression Omnibus (GEO) was utilized to screen for differentially expressed genes. mRNA and protein levels were assessed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis. Flow cytometry was conducted to analyze apoptosis. The levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and malondialdehyde (MDA) were measured using a commercial kit. Dual-luciferase reporter assays and chromatin immunoprecipitation (CHIP) were performed to investigate the interaction between CPB1 and BACH2. The methylation site of BACH2 was analyzed using the RNA-protein binding sites prediction suite and the sequence-based RNA adenosine methylation site predictor suite. Methylated RNA immunoprecipitation (Me-RIP) was employed to detect m6A modification level of BACH2. RESULTS: In ARC and H CONCLUSIONS: METTL3 facilitates apoptosis and oxidative stress in H
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