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ID 48854
フルテキストURL
著者
Sakaguchi, Masakiyo Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Kataoka, Ken Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Abarzua, Fernando Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Tanimoto, Ryuta Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Watanabe, Masami Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Murata, Hitoshi Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Than, Swe Swe Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Kurose, Kaoru Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Kashiwakura, Yuji Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Ochiai, Kazuhiko Innovation Center Okayama for Nanobio-Targeted Therapy, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Nasu, Yasutomo Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Kumon, Hiromi Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
Huh, Nam-ho Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
抄録
We previously showed that the tumor suppressor gene REIC/Dkk-3, when overexpressed by an adenovirus (Ad-REIC), exhibited a dramatic therapeutic effect on human cancers through a mechanism triggered by endoplasmic reticulum stress. Adenovirus vectors show no target cell specificity and thus may elicit unfavorable side effects through infection of normal cells even upon intra-tumoral injection. In this study, we examined possible effects of Ad-REIC on normal cells. We found that infection of normal human fibroblasts (NHF) did not cause apoptosis but induced production of interleukin (IL)-7. The induction was triggered by endoplasmic reticulum stress and mediated through IRE1 alpha, ASK1, p38, and IRF-1. When Ad-REIC-infected NHF were transplanted in a mixture with untreated human prostate cancer cells, the growth of the cancer cells was significantly suppressed. Injection of an IL-7 antibody partially abrogated the suppressive effect of Ad-REIC-infected NHF. These results indicate that Ad-REIC has another arm against human cancer, an indirect host-mediated effect because of overproduction of IL-7 by mis-targeted NHF, in addition to its direct effect on cancer cells.
発行日
2009-05-22
出版物タイトル
The Journal of Biological Chemistry
284巻
21号
出版者
The American Society for Biochemistry and Molecular Biology, Inc.
開始ページ
14236
終了ページ
14244
ISSN
0021-9258
NCID
AA00251083
資料タイプ
学術雑誌論文
プロジェクト
ナノバイオ標的医療の融合的創出拠点
オフィシャル URL
http://www.jbc.org/content/284/21/14236.long
言語
English
著作権者
© 2009 by The American Society for Biochemistry and Molecular Biology, Inc.
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