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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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Title: Suppression of Erk activation and in vivo growth in esophageal cancer cells by the dominant negative Ras mutant, N116Y
Authors: Senmaru, Naoto Browse this author
Shichinohe, Toshiaki Browse this author
Takeuchi, Motoya Browse this author
Miyamoto, Masaki Browse this author
Sazawa, Ataru Browse this author
Ogiso, Yoshifumi Browse this author
Takahashi, Toshiyuki Browse this author
Okushiba, Shyunichi Browse this author
Takimoto, Masato Browse this author
Kato, Hiroyuki Browse this author
Kuzumaki, Noboru11 Browse this author
Authors(alt): 葛巻, 暹11
Issue Date: 29-Oct-1998
Publisher: Wiley-Liss, Inc.
Journal Title: International Journal of Cancer
Volume: 78
Issue: 3
Start Page: 366
End Page: 371
Publisher DOI: 10.1002/(SICI)1097-0215(19981029)78:3<366::AID-IJC18>3.0.CO;2-4
PMID: 09766573
Abstract: 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
Type: article (author version)
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 葛巻 暹

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