World Journal of Oncology, ISSN 1920-4531 print, 1920-454X online, Open Access
Article copyright, the authors; Journal compilation copyright, World J Oncol and Elmer Press Inc
Journal website https://wjon.elmerpub.com

Review

Volume 17, Number 4, August 2026, pages 429-441

RAD51 in Breast Cancer: From Vulnerability to Resistance

Figures

↓  Figure 1. RAD51-mediated homologous recombination versus replication fork protection. The left panel illustrates classical homologous recombination repair initiated following DNA double-strand break formation and BRCA1/MRN/CtIP-mediated end resection, followed by BRCA2-dependent RAD51 loading and recombination-mediated repair. The right panel illustrates replication fork stalling, fork reversal, and RAD51-mediated fork protection during replication stress. Functional separation between homologous recombination repair and replication fork stabilization may contribute to therapeutic resistance in breast cancer.
Figure 1.
↓  Figure 2. Replication fork remodeling and RAD51-mediated fork protection during replication stress. Replication stress induces fork stalling and reversal into a four-way junction structure. BRCA2 promotes RAD51 filament stabilization at reversed forks, protecting nascent DNA from MRE11/DNA2-mediated degradation and facilitating fork restart. In the absence of BRCA2/RAD51-mediated protection, reversed forks undergo nucleolytic degradation, contributing to genomic instability, DNA damage, and cell death.
Figure 2.