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Essential contribution of a chemokine, CCL3, and its receptor, CCR1, to hepatocellular carcinoma progression

フォーマット:
論文
責任表示:
Yang, Xiaoqin ; Lu, Peirong ; Fujii, Chifumi ; Nakamoto, Yasunari ; Gao, Ji Liang ; Kaneko, Shuichi ; Murphy, Philip M. ; Mukaida, Naofumi
言語:
英語
出版情報:
Wiley-Liss, 2006-04-15
著者名:
Yang, Xiaoqin
Lu, Peirong
Fujii, Chifumi
Nakamoto, Yasunari
Gao, Ji Liang
Kaneko, Shuichi
Murphy, Philip M.
Mukaida, Naofumi
続きを見る
掲載情報:
International Journal of Cancer
ISSN:
1097-0215  CiNii Articles  Webcat Plus  JAIRO
巻:
118
通号:
8
開始ページ:
1869
終了ページ:
1876
バージョン:
author
概要:
金沢大学がん研究所がん病態制御<br />We previously observed that a chemokine, macrophage inflammatory protein-1 α/CCL3, and its receptor, CCR1, were aberrantly expressed in human hepatocellular carcinoma (HCC) tissues. Here, we show that CCL3 a nd CCR1 are also expressed in 2 different models of this cancer; N-nitrosodiethylamine (DEN)-induced HCC and HCC induced by hepatitis B virus surface (HBs) antigen-primed splenocyte transfer to myelo-ablated syngeneic HBs antigen transgenic mice. At 10 months after DEN treatment, foci number and sizes were remarkably reduced in CCR1- and CCL3-deficient mice, compared with those of wild-type (WT) mice, although tumor incidence were marginally, but significantly, higher in CCR1- and CCL3-deficient mice than in WT mice. Of note is that tumor angiogenesis was also markedly diminished in CCL3- and CCR1-deficient mice, with a concomitant reduction in the number of intratumoral Kupffer cells, a rich source of growth factors and matrix metalloproteinases (MMPs). Among growth factors and MMPs that we examined, only MMP9 and MMP13 gene expression was augmented progressively in liver of WT mice after DEN treatment. Moreover, MMP9, but not MMP13, gene expression was attenuated in CCR1- and CCL3-deficient mice, compared with that of WT mice. Furthermore, MMP9 was expressed mainly by mononuclear cells but not hepatoma cells, and MMP9-expressing cell numbers were decreased in CCR1- or CCL3-deficient mice, compared with WT mice. These observations suggest the contribution of the CCR1-CCL3 axis to HCC progression. © 2005 Wiley-Liss, Inc. 続きを見る
URL:
http://hdl.handle.net/2297/6666

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