@article{oai:repo.qst.go.jp:00045140,
 author = {Yu, Dong and Sekine, Emiko and Fujimori, Akira and Ochiya, Takahiro and Okayasu, Ryuichi and 于 冬 and 関根 絵美子 and 藤森 亮 and 岡安 隆一},
 issue = {4},
 journal = {Cancer Science},
 month = {Apr},
 note = {In order to study the role of BRCA2 protein in homologous recombination
(HR) repair and radio-sensitization, we utilized RNA interference (RNAi)
strategy in vitro and in vivo with human tumor cells. HeLa cells
transfected with BRCA2 siRNA (Qiagen) as well as negative-control siRNA
for 48 hours were irradiated, and several critical end points were
examined. The radiation cell survival level was significantly reduced in
HeLa cells with BRCA2 siRNA when compared with mock- or negative control
siRNA transfected cells.  DNA double strand break (DSB) repair as
measured by constant field gel-electrophoresis showed a clear inhibition
in cells with BRCA2 siRNA, while little inhibition was observed in cells
with negative control siRNA. Our immuno-staining experiments revealed a
significant delay in Rad51 foci formation in cells with BRCA2 siRNA when
compared with the control populations. However, none of the NHEJ
proteins nor the phosphorylation of DNA-PKcs was affected in cells
transfected with BRCA2 siRNA. In addition, the combined treatment with
radiation and BRCA2 siRNA in xenograft model with HeLa cells showed an
efficient inhibition of in vivo tumor growth. Our results demonstrate
down-regulation of BRCA2 leads to radio-sensitization mainly through the
inhibition of HRR type DSB repair; a possibility of using BRCA2 siRNA as
an effective radiosensitizer in tumor radiotherapy may arise.},
 pages = {810--815},
 title = {Down regulation of BRCA2 causes radio-sensitization of human tumor cells in vitro and in vivo},
 volume = {99},
 year = {2008}
}