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Suppression of Erk activation and in vivo growth in esophageal cancer cells by the dominant negative Ras mutant, N116Y

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タイトル: Suppression of Erk activation and in vivo growth in esophageal cancer cells by the dominant negative Ras mutant, N116Y
著者: Senmaru, Naoto 著作を一覧する
Shichinohe, Toshiaki 著作を一覧する
Takeuchi, Motoya 著作を一覧する
Miyamoto, Masaki 著作を一覧する
Sazawa, Ataru 著作を一覧する
Ogiso, Yoshifumi 著作を一覧する
Takahashi, Toshiyuki 著作を一覧する
Okushiba, Shyunichi 著作を一覧する
Takimoto, Masato 著作を一覧する
Kato, Hiroyuki 著作を一覧する
Kuzumaki, Noboru 著作を一覧する
発行日: 1998年10月29日
出版者: Wiley-Liss, Inc.
誌名: International Journal of Cancer
巻: 78
号: 3
開始ページ: 366
終了ページ: 371
出版社 DOI: 10.1002/(SICI)1097-0215(19981029)78:3<366::AID-IJC18>3.0.CO;2-4
抄録: Our previous studies demonstrated that introduction of a dominant negative H-ras mutant, N116Y, inhibits the growth of various types of cancer cells in vitro. In this study, we tested the efficacy of N116Y in blocking the growth of esophageal cancer cells using an adenoviral vector. Infection with N116Y adenovirus, (AdCMV-N116Y), in which N116Y expression is driven by the cytomegalovirus promoter, significantly reduced the in vitro growth of all esophageal cancer cell lines studied. Esophageal cancer cells that contained wild-type K-ras and H-ras (TE8, SGF3, SGF7) were more sensitive to AdCMV-N116Y than HEC46 cells that expressed mutant K-ras protein.Most importantly, direct injection of AdCMVN116Y into TE8-or SGF3-induced tumors in nude mice suppressed their growth significantly. To examine the suppressive mechanism of N116Y, cell cycle profile and the activation of extracellular signal-regulated kinase 2 (Erk2) were examined by flow cytometry and Western blot analysis, respectively. In TE8 cells, progression into S phase was clearly blocked after infection with AdCMV-N116Y. Infection with AdCMV-N116Y did not strongly suppress the activation of Erk2 after EGF stimulation in serum-starved HEC46 cells, whereas it completely suppressed activation in TE8, SGF3 and SGF7 cells. Our observations suggest that N116Y reduces growth of human esophageal cancer cells and suppresses the activation of Erk2; they also indicate that N116Y is a potential candidate gene for human esophageal cancer gene therapy.
Rights: Copyright (c) 1998 Wiley-Liss, Inc
資料タイプ: article (author version)
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 葛巻 暹


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