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

ABSTRACT: 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

SUBMITTER: Tsai CH 

PROVIDER: S-EPMC6062373 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature