Identification of Id1 as a downstream effector for arsenic-promoted angiogenesis via PI3K/Akt, NF-κB and NOS signaling

Chun Hao Tsai, Ming Hui Yang, Amos C. Hung, Shou Cheng Wu, Wen Chin Chiu, Ming Feng Hou, Yu Chang Tyan, Yun-Ming Wang*, Shyng Shiou F. Yuan

*Corresponding author for this work

研究成果: Article同行評審

5 引文 斯高帕斯(Scopus)

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 μM) 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-κB, 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.

原文English
頁(從 - 到)151-159
頁數9
期刊Toxicology Research
5
發行號1
DOIs
出版狀態Published - 5 十月 2015

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