HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
獣医学研究科  >
雑誌発表論文等  >

Lipophilic triphenylphosphonium derivatives enhance radiation-induced cell killing via inhibition of mitochondrial energy metabolism in tumor cells

この資料はクリエイティブ・コモンズ・ライセンスの下で公開されています。

フルテキスト
Cancer Lett v.390 p.160–167.pdf512.74 kBPDF見る/開く
Supplemental material_Cancer Lett v.390 p.160–167.pdfSupplementary data1.37 MBPDF見る/開く
この文献へのリンクには次のURLを使用してください:http://hdl.handle.net/2115/68704

タイトル: Lipophilic triphenylphosphonium derivatives enhance radiation-induced cell killing via inhibition of mitochondrial energy metabolism in tumor cells
著者: Yasui, Hironobu 著作を一覧する
Yamamoto, Kumiko 著作を一覧する
Suzuki, Motofumi 著作を一覧する
Sakai, Yuri 著作を一覧する
Bo, Tomoki 著作を一覧する
Nagane, Masaki 著作を一覧する
Nishimura, Eri 著作を一覧する
Yamamori, Tohru 著作を一覧する
Yamasaki, Toshihide 著作を一覧する
Yamada, Ken-ichi 著作を一覧する
Inanami, Osamu 著作を一覧する
キーワード: ATP
Cancer
Mitochondria
Radiation
Reactive oxygen species
Triphenylphosphonium
発行日: 2017年 4月 1日
出版者: Elsevier
誌名: Cancer Letters
巻: 390
開始ページ: 160
終了ページ: 167
出版社 DOI: 10.1016/j.canlet.2017.01.006
抄録: It has recently been reported that radiation enhances mitochondrial energy metabolism in various tumor cell lines. To examine how this radiation-induced alteration in mitochondrial function influences tumor cell viability, various lipophilic triphenylphosphonium (TPP+) cation derivatives and related compounds such as 4-hydroxy-2,2,6,6-tetramethyl-1-oxy-piperidin (Tempol) with TPP+ (named “Mito-”) were designed to inhibit the mitochondrial electron transport chain. Mito-(CH2)10-Tempol (M10T) and its derivatives, Mito-(CH2)5-Tempol (M5T), Mito-(CH2)10-Tempol-Methyl (M10T-Me), Mito-C10H21 (M10), and C10H21-Tempol (10T), were prepared. In HeLa human cervical adenocarcinoma cells and A549 human lung carcinoma cells, the fractional uptake of the compound into mitochondria was highest among the TTP+ analogs conjugated with Tempol (M10T, M5T, and 10T). M10T, M10T-Me, and M10 exhibited strong cytotoxicity and enhanced X-irradiation-induced reproductive cell death, while 10T and M5T did not. Furthermore, M10T, M10T-Me, and M10 decreased basal mitochondrial membrane potential and intracellular ATP. M10T treatment inhibited X-ray-induced increases in ATP production. These results indicate that the TPP cation and a long hydrocarbon linker are essential for radiosensitization of tumor cells. The reduction in intracellular ATP by lipophilic TPP+ is partly responsible for the observed radiosensitization. (c) 2017 Elsevier Ireland Ltd. All rights reserved.
Rights: © 2017. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
資料タイプ: article (author version)
URI: http://hdl.handle.net/2115/68704
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 稲波 修

 

本サイトに関するご意見・お問い合わせは repo at lib.hokudai.ac.jp へお願いします。 - 北海道大学