| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2018-01-25 |
| タイトル |
|
|
タイトル |
Angiotensin II enhances epithelial-to-mesenchymal transition through the interaction between activated hepatic stellate cells and the stromal cell-derived factor-1/CXCR4 axis in intrahepatic cholangiocarcinoma |
|
言語 |
en |
| 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 |
| ID登録 |
|
|
ID登録 |
10.24517/00049838 |
|
ID登録タイプ |
JaLC |
| 著者 |
Okamoto, Koichi
Tajima, Hidehiro
Nakanuma, Shinichi
Sakai, Seisho
Makino, Isamu
Kinoshita, Jun
Hayashi, Hironori
Nakamura, Keishi
Oyama, Katsunobu
Nakagawara, Hisatoshi
Fujita, Hideto
Takamura, Hiroyuki
Ninomiya, Itasu
Kitagawa, Hirohisa
Fushida, Sachio
Fujimura, Takashi
Harada, Shinichi
Wakayama, Tomohiko
Iseki, Shoichi
Ohta, Tetsuo
|
| 著者別表示 |
岡本, 浩一
田島, 秀浩
中村, 信一
牧野, 勇
木下, 淳
林, 泰寛
中村, 慶史
尾山, 勝信
中川原, 寿俊
藤田, 秀人
高村, 博之
二宮, 致
北川, 裕久
伏田, 幸夫
藤村, 隆
原田, 真市
若山, 友彦
井関, 尚一
太田, 哲生
|
| 提供者所属 |
|
|
内容記述タイプ |
Other |
|
内容記述 |
金沢大学医薬保健研究域医学系 |
| 書誌情報 |
International Journal of Oncology
巻 41,
号 2,
p. 573-582,
発行日 2012-08
|
| ISSN |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
1019-6439 |
| item_4_source_id_11 |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA10992511 |
| DOI |
|
|
関連タイプ |
isIdenticalTo |
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
10.3892/ijo.2012.1499 |
| 出版者 |
|
|
出版者 |
Spandidos Publications |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
We previously reported that hepatic stellate cells (HSCs) activated by angiotensin II (AngII) facilitate stromal fibrosis and tumor progression in intrahepatic cholangiocarcinoma (ICC). AngII has been known as a growth factor which can promote epithelial-to-mesenchymal transition (EMT) in renal epithelial cells, alveolar epithelial cells and peritoneal mesothelial cells. However, in the past, the relationship between AngII and stromal cell-derived factor-1 (SDF-1) in the microenvironment around cancer and the role of AngII on EMT of cancer cells has not been reported in detail. SDF-1 and its specific receptor, CXCR4, are now receiving attention as a mechanism of cell progression and metastasis. In this study, we examined whether activated HSCs promote tumor fibrogenesis, tumor progression and distant metastasis by mediating EMT via the AngII/AngII type 1 receptor (AT-1) and the SDF-1/CXCR4 axis. Two human ICC cell lines and a human HSC line, LI-90, express CXCR4. Significantly higher concentration of SDF-1αwas released into the supernatant of LI-90 cells to which AngII had been added. SDF-1α increased the proliferative activity of HSCs and enhanced the activation of HSCs as a growth factor. Furthermore, addition of SDF-1α and AngII enhanced the increase of the migratory capability and vimentin expression, reduced E-cadherin expression, and translocated the expression of β-catenin into the nucleus and cytoplasm in ICC cells. Co-culture with HSCs also enhanced the migratory capability of ICC cells. These findings suggest that SDF-1α, released from activated HSCs and AngII, play important roles in cancer progression, tumor fibrogenesis, and migration in autocrine and paracrine fashion by mediating EMT. Our mechanistic findings may provide pivotal insights into the molecular mechanism of the AngII and SDF-1α-initiated signaling pathway that regulates fibrogenesis in cancerous stroma, tumor progression and metastasis of tumor cells expressing AT-1 and CXCR4. |
| 内容記述 |
|
|
内容記述タイプ |
Other |
|
内容記述 |
Embargo Period 6 months |
| 権利 |
|
|
権利情報 |
Copyright © Spandidos Publications |
| 著者版フラグ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
ME-PR-ISEKI-S-573.pdf (737.6 kB)
.png)
