Study on the radiation/heat/anti-cancer drag sensitivity enhanced by siRNA in mutated-p53 cancer cells

本研究的目的是研究NBS1-siRNA或XIAP-siRNA在p53突变的人肺癌细胞中比在野生型p53细胞中更有效地促进放射致敏的机制。本研究表明(1)p53在细胞内与AKT相关，(2)AKT抑制剂（Wortmannin, LY294002）增强了野生型p53和突变型p53细胞的放射敏感性。从这些结果表明，p53和AKT之间的关联是观察到的突变p53细胞的主要放射致敏的原因。

The aim of this study is to examine the mechanism that contributes to radio-sensitization by NBS1-siRNA or XIAP-siRNA observed more effectively in human lung cancer cells having mutated p53 than in those having wild-type p53. This study showed that (1) p53 associates with AKT intracellularly and (2) AKT inhibitors (Wortmannin, LY294002) enhances radio-sensitivity in both of wild-type p53 and mutated p53 cells. From these results it was suggested that the association between p53 and AKT is a cause of the predominant radio-sensitization observed mutated p53 cells.