期刊
CARCINOGENESIS
卷 33, 期 9, 页码 1806-1813出版社
OXFORD UNIV PRESS
DOI: 10.1093/carcin/bgs230
关键词
-
类别
资金
- National Institutes of Health NCI Intramural Research Program
- Center for Cancer Research
- National Institutes of Health [GM065204, CA080946]
Thioredoxin reductase 1 (TR1) controls the redox state of protein thiols in mammalian cells and has been shown to have roles in both preventing and promoting cancer. To define the role of this selenoenzyme in hepatocellular carcinoma development, we examined tumor incidence in the liver of mice with tissue- specific knockout of mouse TR1 subjected to the liver carcinogen, diethylnitrosamine (DEN). TR1- deficient livers manifested 90% tumor incidence compared with 16% in control livers. The TR1- dependent effect was observed independent of sex, and, in control mice, tumorigenesis did not affect the expression of TR1. On the other hand, we observed upregulation of another selenoenzyme, glutathione peroxidase 2 (GPx2), and components of the glutathione (GSH) system, including those that generate reduced GSH. Overall, this study shows that TR1 protects against chemically induced hepatocarcinogenesis via the control of the cellular redox state, whereas its role in promoting this type of cancer is minimal.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据