辐射旁效应在放疗过程中存在增敏和毒副反应的双重作用，其扮演的“双刃剑”角色是影响放疗疗效的关键因素。我们前期研究证实，DNA-PKcs-Chk2调控细胞有丝分裂进程和相关DNA损伤反应蛋白在有丝分裂期的磷酸化，另外，预实验结果显示，不同LET射线照射均可引起处于不同周期状态的细胞产生辐射旁效应，且DNA-PKcs参与细胞周期相关的辐射旁效应，但其具体机制尚不清楚。为此我们提出假设，细胞周期和辐射旁效应密切相关，且很可能受DNA-PKcs-Chk2及其下游通路的调节。为了验证这一假设，本课题拟在前期研究的基础上，围绕“DNA-PKcs-Chk2-细胞周期相关辐射旁效应-增敏和毒副反应”这一主线，从分子，细胞及动物等多方面进行深入探讨，阐明DNA-PKcs-Chk2参与细胞周期相关辐射旁效应的机制，进而为肿瘤放疗策略的制定及挖掘新的潜在治疗靶点提供依据。

Radiation-induced bystander effect (RIBE) comprises dual functions including sensitization and adverse reaction, and this "double-edged sword" role is a key factor that influences the curative effect of cancer radiotherapy. Our preliminary research demonstrated that DNA-PKcs-Chk2 regulated mitosis progression and phosphorylation of DNA damage response protein in mitosis. In addition, pilot studies indicated that RIBE could occur in cells at different cell cycle status in response to various LET radiation, but the underlying mechanisms remain unclear. Therefore, we hypothesized that DNA-PKcs-Chk2 and their downstream factors may regulate cell cycle-related RIBE. To validate our hypothesis, based on our preliminary results, we would like to elucidate the possible mechanisms of the involvement of DNA-PKcs-Chk2 in regulating cell cycle-related RIBE from molecular, cellular and animal levels, providing scientific basis into cancer radiotherapy strategies and excavating potential therapeutic targets.