WEKO3
インデックスリンク
アイテム
Essential contribution of a chemokine, CCL3, and its receptor, CCR1, to hepatocellular carcinoma progression
http://hdl.handle.net/2297/6666
http://hdl.handle.net/2297/666614346b0b-e6e8-48f6-868f-22e852083921
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
CA-PR-MUKIDA-N-1869.pdf (1.1 MB)
|
|
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2017-10-05 | |||||
| タイトル | ||||||
| タイトル | Essential contribution of a chemokine, CCL3, and its receptor, CCR1, to hepatocellular carcinoma progression | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Yang, Xiaoqin
× Yang, Xiaoqin× Lu, Peirong× Fujii, Chifumi× Nakamoto, Yasunari× Gao, Ji Liang× Kaneko, Shuichi× Murphy, Philip M.× Mukaida, Naofumi |
|||||
| 提供者所属 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 金沢大学がん研究所がん病態制御 | |||||
| 書誌情報 |
International Journal of Cancer 巻 118, 号 8, p. 1869-1876, 発行日 2006-04-15 |
|||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1097-0215 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.1002/ijc.21596 | |||||
| 出版者 | ||||||
| 出版者 | Wiley-Liss | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | 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 and 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. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
