Enhanced susceptibility to Fas-mediated apoptosis by interferon-.GAMMA. in an oral squamous cell carcinoma cell line
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- TAKEMI Toshiaki
- Department of Oral and Maxillofacial Surgery, School of Dentistry, Showa University
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- TAKIZAWA Kunio
- Department of Oral and Maxillofacial Surgery, School of Dentistry, Showa University
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- IWASE Masayasu
- Department of Oral and Maxillofacial Surgery, School of Dentistry, Showa University
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- NAGUMO Masao
- Department of Oral and Maxillofacial Surgery, School of Dentistry, Showa University
Bibliographic Information
- Other Title
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- インターフェロン‐γによる口腔へん平上皮癌細胞株のFas誘導アポトーシスへの感受性増強
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Abstract
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.
Journal
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- Japanese Journal of Oral and Maxillofacial Surgery
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Japanese Journal of Oral and Maxillofacial Surgery 50 (11), 629-635, 2004
Japanese Society of Oral and Maxillofacial Surgeons
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Keywords
Details 詳細情報について
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- CRID
- 1390001206533741824
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- NII Article ID
- 10018618714
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- NII Book ID
- AN00189163
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- ISSN
- 21861579
- 00215163
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- Text Lang
- ja
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed