Targeting Ku protein for sensitizing of breast cancer cells to DNA-damage.

Targeting molecular components that are critically involved in the maintenance of genome stability is a promising approach for overcoming intrinsic tumor cell resistance to DNA-damaging treatments. In mammalian cells, the Ku-dependent non-homologous end-joining repair pathway is the predominant process for the repair of double-strand breaks (DSBs) in DNA. Previously, RNA aptamers were selected to efficiently block DNA-binding activity of the Ku protein in vitro.