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. DNA double-strand breaks are lesions induced by ionizing radiation (IR) and can be efficiently repaired by DNA homologous recombination, a system that requires RAD51 recombinase (RAD51). Here we show that overexpression of miR-155 in human breast cancer cells reduces the levels of RAD51 and affects the cellular response to IR. High miR-155 levels were associated with lower RAD51 expression and with better overall survival of patients in a large series of triple-negative breast cancers. Testing triple-negative breast cancer patients for miR-155 expression may be a useful prognostic tool to identify who will benefit from an IR-based therapeutic approach.
- Publication:
-
Proceedings of the National Academy of Science
- Pub Date:
- March 2014
- DOI:
- 10.1073/pnas.1402604111
- Bibcode:
- 2014PNAS..111.4536G