ID | 48854 |
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Sakaguchi, Masakiyo
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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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
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Watanabe, Masami
Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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Murata, Hitoshi
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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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
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Kumon, Hiromi
Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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Huh, Nam-ho
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
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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.
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発行日 | 2009-05-22
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出版物タイトル |
The Journal of Biological Chemistry
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巻 | 284巻
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号 | 21号
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出版者 | The American Society for Biochemistry and Molecular Biology, Inc.
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開始ページ | 14236
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終了ページ | 14244
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ISSN | 0021-9258
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NCID | AA00251083
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資料タイプ |
学術雑誌論文
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プロジェクト |
ナノバイオ標的医療の融合的創出拠点
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オフィシャル URL | http://www.jbc.org/content/284/21/14236.long
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言語 |
英語
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著作権者 | © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.
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論文のバージョン | author
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査読 |
有り
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