Disturbance of DKK1 level is partly involved in survival of lung cancer cells via regulation of ROMO1 and γ-radiation sensitivity

摘要: Dickkopf1 (DKK1), a secreted protein involved in embryonic development, is potent inhibitor of the Wnt signaling pathway and has been postulated to be tumor suppressor or promoter depending on type. In this study, we showed that DKK1 was expressed differently among non-small-cell lung cancer cell lines. The expression level much higher A549 cells than H460 cells. We revealed blockage by silencing RNA caused up-regulation intracellular reactive oxygen species (ROS) modulator (ROMO1) protein, followed partial death, growth inhibition, loss epithelial–mesenchymal transition property ROS, it also increased γ-radiation sensitivity. overexpression significantly inhibited survival with decrease ROMO1 level, which induced cellular ROS. Thereafter, exogenous N-acetylcysteine, an antioxidant, hydrogen peroxide, pro-oxidant, partially rescued from death inhibition. each line, both not only elevated p-RB activation, led arrest, but inactivated AKT/NF-kB, radiation sensitivity growth. This study first demonstrate strict modulation different types maintains via tight regulation ROS-producing resistance.