インターフェロン-γによる口腔扁平上皮癌細胞株の Fas 誘導アポトーシスへの感受性増強 Enhanced susceptibility to Fas-medicated apoptosis by interferon-γ in an oral squamous cell carcinoma cell line

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著者

    • 竹味 利晃 TAKEMI Toshiaki
    • 昭和大学歯学部顎口腔疾患制御外科学教室 Department of Oral and Maxillofacial Surgery, School of Dentistry, Showa University
    • 滝沢 邦生 TAKIZAWA Kunio
    • 昭和大学歯学部顎口腔疾患制御外科学教室 Department of Oral and Maxillofacial Surgery, School of Dentistry, Showa University
    • 岩瀬 正泰 IWASE Masayasu
    • 昭和大学歯学部顎口腔疾患制御外科学教室 Department of Oral and Maxillofacial Surgery, School of Dentistry, Showa University
    • 南雲 正男 NAGUMO Masao
    • 昭和大学歯学部顎口腔疾患制御外科学教室 Department of Oral and Maxillofacial Surgery, School of Dentistry, Showa University

抄録

Fas is widely expressed on the cell surface of many normal and neoplastic cells and induces apoptotic cell death in the presence of Fas ligand (FasL) or Fas-agonistic antibody CH11 (Fas-mediated apoptosis) Cancer cells constitutively expressing Fas are generally resistant to Fas-mediatedapoptosis. Recently, it has been reported that interferon-γ(IFN-γ) enhances Fas-mediated apoptosis. An oral squamous cell carcinoma cell line, NA, also constitutively expresses Fas on the plasma membrane and shows low susceptibility to Fas-agonistic antibody-induced apoptosis. This study was conducted to examine the effects of IFN-γ on Fas-mediated apoptosis, the expression of Fas and FasL, and the production of soluble Fas (sFas) in NA cells. The results revealed that a Fas-agonistic antibody, CH11, induced apoptosis of NA cells and IFN-γ enhanced susceptibility of NA cells to CH11-induced apoptosis. Further more, IFN-γ up-regulated Fas expression on NA cells without affecting the expression of FasL. A slight decrease in sFas expression was induced by treatment with IFN-γ. These results suggest that IFN-γ may enhance the susceptibility of NA cells to Fas-mediated apoptosis through the up-regulation of Fas.

収録刊行物

  • 日本口腔外科学会雑誌  

    日本口腔外科学会雑誌 50(11), 629-635, 2004-11-20 

    Japanese Society of Oral and Maxillofacial Surgeons

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各種コード

  • NII論文ID(NAID)
    10018618714
  • NII書誌ID(NCID)
    AN00189163
  • 本文言語コード
    JPN
  • 資料種別
    ART
  • ISSN
    00215163
  • データ提供元
    CJP書誌  J-STAGE 
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