摘要
DNA-dependent protein kinase catalytic subunit(DNA-PKcs)plays a critical role in non-homologous end joining(NHEJ)of DNA double-stand break(DSB)repair.Previously,we found genistein could sensitize cancer cells to low linear energy transfer(LET)X-rays via inhibiting DNA-PKcs activities.Especially,high-LET heavy ion produces more DNA DSBs than low-LET radiation.Presently,we demonstrated that DNA-PKcs specific inhibitor Nu7026 treatment or siRNA knockdown of DNA-PKcs could sensitize DNA-PKcs proficient glioblastoma cells to high-LET carbon ions(shown in Table 1).Immunofluorescence and western blot experiments were performed to examine the DNA DSBs and their repair kinetics in two DNA-PKcs proficient glioblastoma cell lines.
