@article{oai:repo.qst.go.jp:00043138,
 author = {Peng, Yuanlin and Zhang, Qinming and Nagasawa, Hatsumi and Okayasu, Ryuichi and L., Liber Howard and S., Bedford Joel and 岡安 隆一},
 journal = {Cancer Research},
 month = {Nov},
 note = {Targeted gene silencing in mammalian cells by RNA interference (RNAi) using small interfering RNAs (siRNAs) was recently described by Elbashir et al. (S.M. Elbashir et al., Nature (Lond.), 411: 494-498, 2001).  We have used this methodology in several human cell strains to reduce expression of Prkdc (DNA-PKcs) gene coding for the catalytic sub-unit of the DNA-dependent protein kinase (DNA-PKcs), that is involved in the nonhomologous end joining (NHEJ) of DNA double strand breaks.  We have also demonstrated a radiosensitization for several phenotypic endpoints of radiation damage.  In low passage normal human fibroblasts, siRNA knock-down of DNA-PKcs resulted in a reduced capacity for restitution of radiation-induced interphase chromosome breaks as measured by premature chromosome condensation (PCC), an increased yield of acentric chromosome fragments at the first post-irradiation mitosis, and an increased radiosensitivity for cell killing.  For three strains of related human lymphoblasts, DNA-PKcs targeted siRNA transfection resulted in little or no increase in radiosensitivity with respect to cell killing, a 1.5-fold decrease in induced mutant yield in TK6 and p53-null NH32 cells, but about a 2-fold increase in induced mutant yield in p53 mutant WTK1 cells at both the hypoxanthine quinine phosphoribosyl transferase (hprt) and the thymidine kinase loci.},
 pages = {6400--6404},
 title = {Silencing expression of the catalytic subunit of DNA-dependent protein kinase by small interfering RNA sensitizes human Cells for radiation-induced chromosome damage, cell killing and mutation},
 volume = {62},
 year = {2002}
}