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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
https://repo.qst.go.jp/records/65507
https://repo.qst.go.jp/records/6550755c80727-1fca-468f-bea6-172e721eed11
Item type | 会議発表用資料 / Presentation(1) | |||||
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公開日 | 2014-09-30 | |||||
タイトル | ||||||
タイトル | 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 | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
資源タイプ | conference object | |||||
アクセス権 | ||||||
アクセス権 | metadata only access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
著者 |
藤田, 真由美
× 藤田, 真由美× 山田, 滋× 今井, 高志× 藤田 真由美× 山田 滋× 今井 高志 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 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. | |||||
会議概要(会議名, 開催地, 会期, 主催者等) | ||||||
内容記述タイプ | Other | |||||
内容記述 | 第73回日本癌学会学術総会 | |||||
発表年月日 | ||||||
日付 | 2014-09-26 | |||||
日付タイプ | Issued |