PBX1 attenuates MeHg-induced apoptosis by reducing ROS accumulation, mitigating double-strand DNA breaks, and enhancing homologous recombination DNA repair in SH-SY5Y cells

Given the critical role of PBX1 in maintaining genomic stability and the well-documented DNA damage effects of methylmercury (MeHg) in SH-SY5Y cells, we hypothesize that PBX1 overexpression may alleviate MeHg-induced ROS accumulation, DNA damage, and apoptosis in SH-SY5Y cells by enhancing the homologous recombination (HR) repair pathway. To test this hypothesis, we generated PBX1-overexpressing cells via lentiviral packaging.

Cell viability was assessed using MTT assay, while ROS levels and apoptosis were measured by flow cytometry. DNA damage was evaluated through comet assay, and the binding of PBX1 to the BRCA1 promoter region was examined using dual-luciferase reporter assay. The expression of damage repair and apoptosis-related proteins was detected by Western blotting.