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Accelerated hepatocellular carcinoma development in mice expressing the Pim-3 transgene selectively in the liver

フォーマット:
論文
責任表示:
Wu, Yu ; Wang, Ying Ying ; Nakamoto, Yasunari ; Li, Ying-Yi ; Baba, Tomohisa ; Kaneko, Shuichi ; Fujii, Chifumi ; Mukaida, Naofumi
言語:
英語
出版情報:
Nature Publishing Group, 2010-04-01
著者名:
Wu, Yu
Wang, Ying Ying
Nakamoto, Yasunari
Li, Ying-Yi
Baba, Tomohisa
Kaneko, Shuichi
Fujii, Chifumi
Mukaida, Naofumi
続きを見る
掲載情報:
Oncogene
ISSN:
0950-9232  CiNii Articles  Webcat Plus  JAIRO
巻:
29
通号:
15
開始ページ:
2228
終了ページ:
2237
バージョン:
author
概要:
金沢大学がん研究所<br />Pim-3, a proto-oncogene with serine/threonine kinase activity, was enhanced in hepatocellular carcinoma (HCC) tissues. To address the roles of Pim-3 in HCC development, we prepared transgenic mice that express human Pim -3 selectively in liver. The mice were born at a Mendelian ratio, were fertile and did not exhibit any apparent pathological changes in the liver until 1 year after birth. Pim-3-transgenic mouse-derived hepatocytes exhibited accelerated cell cycle progression. The administration of a potent hepatocarcinogen, diethylnitrosamine (DEN), induced accelerated proliferation of liver cells in Pim-3 transgenic mice in the early phase, compared with that observed for wild-type mice. Treatment with DEN induced lipid droplet accumulation with increased proliferating cell numbers 6 months after the treatment. Eventually, wild-type mice developed HCC with a frequency of 40% until 10 month after the treatment. Lipid accumulation was accelerated in Pim-3 transgenic mice with higher proliferating cell numbers, compared with that observed for wild-type mice. Pim-3 transgenic mice developed HCC with a higher incidence (80%) and a heavier burden, together with enhanced intratumoral CD31-positive vascular areas, compared with that observed for wild-type mice. These observations indicate that Pim-3 alone cannot cause, but can accelerate HCC development when induced by a hepatocarcinogen, such as DEN. © 2010 Macmillan Publishers Limited. All rights reserved. 続きを見る
URL:
http://hdl.handle.net/2297/24282

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