Signaling by carcinogenic metals and metal-induced reactive oxygen species.
Epidemiological data indicate that exposure to metal and metalloid species, including arsenic(III), chromium(VI), and nickel(II), increases the risk of cancer, particularly of the lung and skin. Alterations in normal signal transduction as a result of exposure to carcinogenic metals, and to metal-catalyzed reactive oxygen species (ROS) formation, appear to play an important role in the etiology of metal-induced carcinogenesis. Signaling components affected by metals include growth factor receptors, G-proteins, MAP kinases, and nuclear transcription factors. This article reviews current literature on the effects of carcinogenic metals and metal-induced ROS on cancer-related signaling pathways. In addition, the mechanisms by which those changes occur, and the role of those changes in carcinogenesis are discussed.
Harris
Gabriel Keith
GK
National Research Council Associate, Pathology and Physiology Research Branch, National Institute for Occupational Safety and Health, 1095 Willowdale Rd. (M/S 2015), Morgantown, WV 26505-2888, USA. gharris1@cdc.gov
Shi
Xianglin
X
D000818:Animals; D002273:Carcinogens / Q000633:toxicity*; D006801:Humans; D008670:Metals / Q000633:toxicity*; D009369:Neoplasms / Q000139:chemically induced / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species / Q000633:toxicity*; D015398:Signal Transduction / Q000187:drug effects*
D002273:Carcinogens; D008670:Metals; D017382:Reactive Oxygen Species