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タイトル: Angiotensin II induces tumor progression and fibrosis in intrahepatic cholangiocarcinoma through an interaction with hepatic stellate cells
著者: Okamoto, Koichi
Tajima, Hidehiro
Ohta, Tetsuo link image link image
Nakanuma, Shinichi
Hayashi, Hironori link image link image
Nakagawara, Hisatoshi
Onishi, Ichiro
Takamura, Hiroyuki link image link image
Ninomiya, Itasu link image link image
Kitagawa, Hirohisa
Fushida, Sachio link image link image
Tani, Takashi link image link image
Fujimura, Takashi
Kayahara, Masato
Harada, Shinichi link image link image
Wakayama, Tomohiko
Iseki, Shoichi link image
岡本, 浩一
太田, 哲生
中沼, 安二
林, 泰寛
大西, 一朗
高村, 博之
北川, 裕久
伏田, 幸夫
谷, 卓
藤村, 隆
萱原, 正都
原田, 真市
若山, 友彦
井関, 尚一
発行日: 2010年11月
出版社(者): Spandidos Publications
雑誌名: International Journal of Oncology
ISSN: 1019-6439
巻: 37
号: 5
開始ページ: 1251
終了ページ: 1259
キーワード: Angiotensin II
Angiotensin II type 1 receptor
Hepatic stellate cell
Intrahepatic cholangiocarcinoma
抄録: Intrahepatic cholangiocarcinoma (ICC) is characterized as a highly fatal tumor with poor prognosis because of its strong progression, early invasion, widespread metastasis and rich cancerous stroma. Although it is widely accepted that fibroblasts facilitate stromal fibrosis and tumor progression, the mechanisms of the interaction between cancer cells and activated fibroblasts have not been fully elucidated thus far. In this study, we demonstrate the presence of angiotensin II (AngII) in ICC tissues and explore the interaction between hepatic stellate cells (HSCs) and ICC cells as one of the sources of stromal fibrosis and tumor progression through the interaction of the AngII/AngII type 1 receptor (AT-1) axis. The concentrations of AngII in ICC tissues were significantly higher than those of HCC and normal liver. Two human ICC cell lines (HuCCT-1, CCKS-1) and a human HSC cell line (LI-90) expressed AT-1 mRNA and protein. The proliferative activity of ICC cells and HSCs to which AngII was added dose-dependently increased and AT-1 antagonist inhibited the proliferative effects. HSCs to which AngII was added showed a higher expression of α-smooth muscle actin (α-SMA, a marker of activated HSCs and myofibroblasts), glial fibrillary acidic protein (GFAP, a specific marker of HSCs) and collagen type I than control cells. AT-1 antagonist also inhibited the activation and transformation of HSCs stimulated by AngII. These findings suggested that locally formed AngII in ICC tissues plays a role in the proliferation and activation of ICC cells and HSCs expressing AT-1 as a growth factor in autocrine and paracrine fashions. Our mechanistic findings provide the first insight into an autocrine and paracrine AngII-initiated signaling pathway that regulates ICC proliferation and fibrosis.
DOI: 10.3892/ijo-00000776
URI: http://hdl.handle.net/2297/25424
資料種別: Journal Article
版表示: publisher
出現コレクション:1. 査読済論文

このアイテムを引用あるいはリンクする場合は次の識別子を使用してください。 http://hdl.handle.net/2297/25424



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