@misc{oai:repo.qst.go.jp:00069026,
 author = {Yu, Dong and Sekine, Emiko and Ninomiya, Yasuharu and Fujimori, Akira and Okayasu, Ryuichi and et.al and 于 冬 and 関根 絵美子 and 二宮 康晴 and 藤森 亮 and 岡安 隆一},
 month = {Jul},
 note = {Heat-shock protein 90 (Hsp90) is a ubiquitous molecular chaperone protein, which is related to the stabilization and activation of various cell cycle checkpoints and signal transduction proteins. An effective Hsp90 inhibitor 17-AAG has now entered clinical trials. Insulin-like growth factor I receptor (IGF-IR) over-expressed HeLa cells (HeLa-IGF-IR) exhibit a radioresistant phenotype and are difficult to be treated with radio-therapy. We studied the radio-sensitization effects of 17-AAG in HeLa-IGF-IR cells. After pretreatment with 17-AAG for 24 hours, characteristics of irradiated cells were examined by colony-forming assay, MTT assay, western blotting, and immunostaining. 150nM of 17-AAG pretreatment significantly radio-sensitized HeLa-IGF-IR cells, but this sensitization was not observed with non-transfected HeLa cells. The protein expression of PARP after irradiation was reduced with 17-AAG pretreatment, indicating an increase in apoptosis formation. Irradiation with 17-AAG pretreatment in HeLa-IGF-IR cells led to reduction in cell growth kinetics when compared to HeLa cells. The downstream pathways of IGF-IR (PI3-K/Akt and Raf/MEK/ERK pathways, proliferation signal pathways) were inhibited by 17-AAG treatment, and more cells were led to apoptosis. We also used the tumor xenografts model using SQ5 lung carcinoma cells to examine the antitumor effect of 17-AAG in vivo. The combined treatment with 17-AAG (80mg/kg, 1-3 times/week, i.p.) and 8 Gy gamma-rays significantly inhibited tumor growth. 17AAG treatment would be a useful method for certain radio-resistant tumor cells., 13th International Congress of Radiation Research},
 title = {Radio-sensitization by 17AAG in human tumor cells},
 year = {2007}
}