Protective role of miR-155 in breast cancer through RAD51 targeting impairs homologous recombination after irradiation.

ABSTRACT: Cell survival after DNA damage relies on DNA repair, the abrogation of which causes genomic instability and development of cancer. However, defective DNA repair in cancer cells can be exploited for cancer therapy using DNA-damaging agents. DNA double-strand breaks are the major lethal lesions induced by ionizing radiation (IR) and can be efficiently repaired by DNA homologous recombination, a system that requires numerous factors including the recombinase RAD51 (RAD51). Therapies combined with adjuvant radiotherapy have been demonstrated to improve the survival of triple-negative breast cancer patients; however, such therapy is challenged by the emergence of resistance in tumor cells. It is, therefore, essential to develop novel therapeutic strategies to overcome radioresistance and improv

SUBMITTER: Gasparini P 

PROVIDER: S-EPMC3970505 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature