@misc{oai:repo.qst.go.jp:00065507,
 author = {藤田, 真由美 and 山田, 滋 and 今井, 高志 and 藤田 真由美 and 山田 滋 and 今井 高志},
 month = {Sep},
 note = {We previously demonstrated that 2 or 4 Gy of X-ray irradiation induced MIAPaCa-2 invasiveness, whereas 0.5, 1, 2, or 4 Gy of carbon-ion (C-ion) suppressed invasion. ROCK inhibitor in addition to MMP-2 inhibitor was needed to suppress MIAPaCa-2 invasion indicated both mesenchymal and amoeboid modes of motility were functioned. Here we show that 2 Gy of C-ion irradiation reduced GTP-bound Rac1 and RhoA expression, the active form of Rac1 and RhoA, which are the key factors involved in two modes of motility. The reduction of GTP-bound Rac1 or RhoA was recovered by the treatment of proteasome inhibitor, indicated that those proteins were undergo degradation via the ubiquitin-proteasome pathway. So far, IAPs, Inhibitors of Apoptosis Proteins, and HACE1, HECT-domain containing E3 ubiquitin-ligase, were reported as a direct E3 ubiquitin ligase of Rac1. Of those, XIAP was selectively induced after C-ion irradiation. In addition, XIAP was co-precipitated with GTP-bound Rac1 in C-ion irradiated MIAPaCa-2. In conclusion, unlike X-ray irradiation, C-ion irradiation inhibited both mesenchymal and amoeboid motility via GTP-bound Rac1 and RhoA degradation, causing effective reduction of invasion., 第73回日本癌学会学術総会},
 title = {炭素線照射はGTP-bound Rac1 とRhoA のタンパク分解を介し膵癌由来細胞株MIAPaCa-2 の浸潤能を抑制する},
 year = {2014}
}