標題: Identification of Id1 as a downstream effector for arsenic-promoted angiogenesis via PI3K/Akt, NF-kappa B and NOS signaling
作者: Tsai, Chun-Hao
Yang, Ming-Hui
Hung, Amos C.
Wu, Shou-Cheng
Chiu, Wen-Chin
Hou, Ming-Feng
Tyan, Yu-Chang
Wang, Yun-Ming
Yuan, Shyng-Shiou F.
生物科技學系
分子醫學與生物工程研究所
Department of Biological Science and Technology
Institute of Molecular Medicine and Bioengineering
公開日期: 1-Jan-2016
摘要: Exposure to arsenic is known to be a risk factor for various types of cancer. Apart from its carcinogenic activity, arsenic also shows promoting effects on angiogenesis, a crucial process for tumor growth. Yet, the mechanism underlying arsenic-induced angiogenesis is not fully understood. In this study, we aimed at investigating the involvement of inhibitor of DNA binding 1 (Id1) and the associated signal molecules in the arsenic-mediated angiogenesis. Our initial screening revealed that treatment with low concentrations of arsenic (0.5-1 mu M) led to multiple cellular responses, including enhanced endothelial cell viability and angiogenic activity as well as increased protein expression of Id1. The arsenic-induced angiogenesis was suppressed in the Id1-knocked down cells compared to that in control cells. Furthermore, arsenic-induced Id1 expression and angiogenic activity were regulated by PI3K/Akt, NF-kappa B, and nitric oxide synthase (NOS) signaling. In summary, our current data demonstrate for the first time that Id1 mediates the arsenic-promoted angiogenesis, and Id1 may be regarded as an antiangiogenesis target for treatment of arsenic-associated cancer.
URI: http://dx.doi.org/10.1039/c5tx00280j
http://hdl.handle.net/11536/129520
ISSN: 2045-452X
DOI: 10.1039/c5tx00280j
期刊: TOXICOLOGY RESEARCH
起始頁: 151
結束頁: 159
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