New perspectives in arsenic-induced cell signal transduction.
Although the carcinogenicity of arsenic has been well established, the underlying molecular mechanisms have not yet been fully identified. Accumulating evidence indicates that the alteration of cellular signal transduction is directly related to the carcinogenesis of arsenic. This review focuses on recent advances in arsenic-induced signal transduction, including reactive oxygen species (ROS) production, tyrosine phosphorylation, MAPK signaling, NF-kappaB activation, cell cycle arrest, and apoptosis.
Qian
Yong
Y
Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26506, USA. yqian@cdc.gov
Castranova
Vince
V
Shi
Xianglin
X
D017209:Apoptosis / Q000187:drug effects; D001151:Arsenic / Q000494:pharmacology*; D001152:Arsenicals / Q000494:pharmacology; D002273:Carcinogens / Q000494:pharmacology; D002453:Cell Cycle / Q000187:drug effects; D006801:Humans; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*
D001152:Arsenicals; D002273:Carcinogens; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D020929:Mitogen-Activated Protein Kinase Kinases; D001151:Arsenic