MISC

2017年

Tumor-Associated Macrophages in the Development of 4-Nitroquinoline-1-Oxide-Induced Tongue Squamous Cell Carcinoma in a Mouse Model

ONCOLOGY
  • Kentaro Miki
  • ,
  • Yorihisa Orita
  • ,
  • Yuka Gion
  • ,
  • Soshi Takao
  • ,
  • Kyotaro Ohno
  • ,
  • Mai Takeuchi
  • ,
  • Toshihiro Ito
  • ,
  • Akira Minoura
  • ,
  • Tomoyasu Tachibana
  • ,
  • Hidenori Marunaka
  • ,
  • Takuma Makino
  • ,
  • Akihiro Matsukawa
  • ,
  • Kazunori Nishizaki
  • ,
  • Tadashi Yoshino
  • ,
  • Yasuharu Sato

93
3
開始ページ
204
終了ページ
212
記述言語
英語
掲載種別
DOI
10.1159/000477301
出版者・発行元
KARGER

Objective: We aimed to determine the distribution of tumor-associated macrophages (TAMs) in the development of tongue squamous cell carcinoma (SCC) and to elucidate the role of TAMs in the progression of tongue SCC. Methods: The expression of the macrophage markers nitric oxide synthase, Retnla, and mannose receptor 1 in the development of tongue SCC was longitudinally observed using real-time quantitative polymerase chain reaction. Additionally, an immunohistochemical study using an anti-mannose receptor (MR) antibody was performed. Results: The numbers of both of M1 and M2 macrophages in the tongues of mice treated with 4-nitroquinoline-1-oxide (4NQO) were significantly lower compared with those of normal tongues. The cyclo-oxygenase-2 (COX-2) inhibitor did not prevent cancer progression and did not affect the total number of macrophages in the tongues of 4NQO-treated mice. In the immunohistochemical studies, MR staining was observed in lymphangio-endothelium in the subepithelial area of the tongues. The staining intensity of the MR was significantly stronger in the 4NQO-treated mice compared with that in control mice and 4NQO-treated mice treated with the COX-2 inhibitor. Conclusion: TAMs may not contribute to the development of 4NQO-induced tongue SCC. MR expression is associated with the progression of 4NQO-induced tongue SCC. (C) 2017 S. Karger AG, Basel


リンク情報
DOI
https://doi.org/10.1159/000477301
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000408964000008&DestApp=WOS_CPL
ID情報
  • DOI : 10.1159/000477301
  • ISSN : 0030-2414
  • eISSN : 1423-0232
  • Web of Science ID : WOS:000408964000008

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