RNF8: POTENTIAL THERAPEUTIC TARGET FOR BREAST CANCER TREATMENT?

Hereditary breast cancer has been associated with alterations in the BRCA1 gene, making it impossible to repair DNA double-strand breaks by homologous recombination. This condition involves 53BP1, frequently altered in cancer, which function is essential for the non-homologous end joining mechanism, promoting genomic instability and mammary tumorigenesis. RNF8 is an E3 ubiquitin-protein ligase whose function promotes the binding of BRCA1 and 53BP1 locating them at sites of DNA damage. Some approaches are presented with the aim to recognize and promote the elimination of RNF8, which could be used as a pharmacological strategy to eliminate both the 53BP1-dependent genomic instability and drug resistance promoted by its inactivation in BRCA1-deficient mammary cells.