Enhanced Homologous Recombination via Rad51 Modulation in DNA Repair of Human Fibroblasts

DNA repair is a critical process that maintains genomic stability and protects against carcinogenesis. The modulation of homologous recombination (HR) pathways has shown promise in enhancing DNA repair fidelity. This study aims to elucidate the role of Rad51 protein in promoting efficient HR-mediated DNA repair in human fibroblasts. Using CRISPR/Cas9 technology, we engineered fibroblast cell lines with upregulated Rad51 expression. We employed fluorescent tagging and confocal microscopy to track DNA repair dynamics and utilized quantitative PCR to measure repair efficiency. Our findings indicate that Rad51 overexpression resulted in a significant increase in HR activity, with a 35% improvement in repair efficiency compared to controls (p < 0.01). Furthermore, Rad51-modulated cells exhibited enhanced resistance to DNA-damaging agents, reducing cell death by 40%. These results suggest that Rad51 is a pivotal factor in optimizing HR pathways, providing a potential therapeutic target for enhancing DNA repair in various diseases. The study underscores the importance of modulating specific proteins to improve genomic integrity, with implications for cancer treatment and cell therapy.