期刊
TOXICOLOGY AND APPLIED PHARMACOLOGY
卷 256, 期 2, 页码 114-121出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2011.07.016
关键词
Arsenic; Reactive oxygen species; NADPH oxidase; beta-catenin; Cell transformation; Tumorigenesis
资金
- NIH [R01CA119028, R01CA116697, R01ES015375, R01ES015518]
Long term exposure to arsenic can increase incidence of human cancers, such as skin, lung, and colon rectum. The mechanism of arsenic induced carcinogenesis is still unclear. It is generally believed that reactive oxygen species (ROS) may play an important role in this process. In the present study, we investigate the possible linkage between ROS, beta-catenin and arsenic induced transformation and tumorigenesis in human colorectal adenocarcinoma cell line, DLD1 cells. Our results show that arsenic was able to activate p47(phox) and p67(phox), two key proteins for activation of NADPH oxidase. Arsenic was also able to generate ROS in DLD1 cells. Arsenic increased beta-catenin expression level and its promoter activity. ROS played a major role in arsenic-induced beta-catenin activation. Treatment of DLD1 cells by arsenic enhanced both transformation and tumorigenesis of these cells. The tumor volumes of arsenic treated group were much larger than those without arsenic treatment. Addition of either superoxide dismutase (SOD) or catalase reduced arsenic induced cell transformation and tumor formation. The results indicate that ROS are involved in arsenic induced cell transformation and tumor formation possible through Wnt/beta-catenin pathway in human colorectal adenocarcinoma cell line DLD1 cells. (C) 2011 Published by Elsevier Inc.
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