目的观察60Co照射后体外培养的食管癌细胞株TE-13和ECA109细胞中MDC1和53BP1蛋白表达、ECA109细胞核内MDC1和53BP1斑点数量的变化,探讨放射线对食管癌细胞中相关蛋白表达的影响。方法 Western blot检测照射后细胞中MDC1和53BP1蛋白表达...目的观察60Co照射后体外培养的食管癌细胞株TE-13和ECA109细胞中MDC1和53BP1蛋白表达、ECA109细胞核内MDC1和53BP1斑点数量的变化,探讨放射线对食管癌细胞中相关蛋白表达的影响。方法 Western blot检测照射后细胞中MDC1和53BP1蛋白表达,激光共聚焦显微镜观察放射线照射后食管癌细胞ECA109中MDC1和53BP1细胞核内斑点数量的变化。结果 0、1、2、5、10Gy照射后1、2、24h,TE-13和ECA109细胞MDC1和53BP1蛋白表达未见明显变化(P>0.05);细胞接受不同剂量放射线照射后1h,MDC1和53BP1核内斑点的数量呈现明显剂量依赖性,与对照组(0Gy组)相比,差异具有统计学意义(P<0.05);同时发现4Gy放射线照射后30min(MDC1)～1h(53BP1)细胞核内斑点的数量最多,分别为26.3和36.7个,其后斑点的数量逐渐下降,与对照组(0Gy组)相比,差异均具有统计学意义(P<0.05)。结论单纯放射线照射未发现食管癌细胞中MDC1和53BP1蛋白表达发生明显变化,但两种蛋白在细胞核内斑点的数量与剂量和照射后时间存在明显的量效关系。展开更多
Maintenance of cellular homeostasis and genome integrity is a critical responsibility of DNA double-strand break(DSB)signaling.P53-binding protein 1(53BP1)plays a critical role in coordinating the DSB repair pathway c...Maintenance of cellular homeostasis and genome integrity is a critical responsibility of DNA double-strand break(DSB)signaling.P53-binding protein 1(53BP1)plays a critical role in coordinating the DSB repair pathway choice and promotes the non-homologous end-joining(NHEJ)-mediated DSB repair pathway that rejoins DSB ends.New insights have been gained into a basic molecular mechanism that is involved in 53BP1 recruitment to the DNA lesion and how 53BP1 then recruits the DNA break-responsive effectors that promote NHEJ-mediated DSB repair while inhibiting homologous recombination(HR)signaling.This review focuses on the up-and downstream pathways of 53BP1 and how 53BP1 promotes NHEJ-mediated DSB repair,which in turn promotes the sensitivity of poly(ADP-ribose)polymerase inhibitor(PARPi)in BRCA1-deficient cancers and consequently provides an avenue for improving cancer therapy strategies.展开更多
文摘目的观察60Co照射后体外培养的食管癌细胞株TE-13和ECA109细胞中MDC1和53BP1蛋白表达、ECA109细胞核内MDC1和53BP1斑点数量的变化,探讨放射线对食管癌细胞中相关蛋白表达的影响。方法 Western blot检测照射后细胞中MDC1和53BP1蛋白表达,激光共聚焦显微镜观察放射线照射后食管癌细胞ECA109中MDC1和53BP1细胞核内斑点数量的变化。结果 0、1、2、5、10Gy照射后1、2、24h,TE-13和ECA109细胞MDC1和53BP1蛋白表达未见明显变化(P>0.05);细胞接受不同剂量放射线照射后1h,MDC1和53BP1核内斑点的数量呈现明显剂量依赖性,与对照组(0Gy组)相比,差异具有统计学意义(P<0.05);同时发现4Gy放射线照射后30min(MDC1)～1h(53BP1)细胞核内斑点的数量最多,分别为26.3和36.7个,其后斑点的数量逐渐下降,与对照组(0Gy组)相比,差异均具有统计学意义(P<0.05)。结论单纯放射线照射未发现食管癌细胞中MDC1和53BP1蛋白表达发生明显变化,但两种蛋白在细胞核内斑点的数量与剂量和照射后时间存在明显的量效关系。
文摘Maintenance of cellular homeostasis and genome integrity is a critical responsibility of DNA double-strand break(DSB)signaling.P53-binding protein 1(53BP1)plays a critical role in coordinating the DSB repair pathway choice and promotes the non-homologous end-joining(NHEJ)-mediated DSB repair pathway that rejoins DSB ends.New insights have been gained into a basic molecular mechanism that is involved in 53BP1 recruitment to the DNA lesion and how 53BP1 then recruits the DNA break-responsive effectors that promote NHEJ-mediated DSB repair while inhibiting homologous recombination(HR)signaling.This review focuses on the up-and downstream pathways of 53BP1 and how 53BP1 promotes NHEJ-mediated DSB repair,which in turn promotes the sensitivity of poly(ADP-ribose)polymerase inhibitor(PARPi)in BRCA1-deficient cancers and consequently provides an avenue for improving cancer therapy strategies.
