Activation of nuclear factor-kappaB and not activator protein-1 in cellular response to nickel compounds.
The predominant exposure route for nickel compounds is by inhalation, and several studies have indicated the correlation between nickel exposure and respiratory cancers. The tumor-promoting effects of nickel compounds are thought to be associated with their transactivation of transcription factors. We have investigated the possible activation of activator protein-1 (AP-1) and nuclear factor KB (NF-kappaB) in mouse C141 epidermal cells and fibroblasts 3T3 and B82, and human bronchoepithelial BEAS-2B cells in response to nickel compound exposure. Our results show that NF-kappaB activity is induced by nickel exposure in 3T3 and BEAS-2B cells. Conversely, similar nickel treatment of these cells did not induce AP-1 activity, suggesting that nickel tumorigenesis occurs through NF-kappaB and not AP-1. We also investigated the role of NF-kappaB in the induction of Cap43 by nickel compounds using dominant negative mutant Ikappabeta kinase b-KM BEAS-2B transfectants.
Huang
Yi
Y
Monroe-Woodbury High School, Central Valley, New York, USA.
Davidson
Gerard
G
Li
Jingxia
J
Yan
Yan
Y
Chen
Fei
F
Costa
Max
M
Chen
Lung Chi
LC
Huang
Chuanshu
C
D000818:Animals; D018929:Cell Culture Techniques; D005347:Fibroblasts; D006801:Humans; D019570:Inhalation Exposure; D008168:Lung / Q000166:cytology; D051379:Mice; D016328:NF-kappa B / Q000096:biosynthesis*; D009532:Nickel / Q000009:adverse effects*; D010957:Plasmids; D012867:Skin / Q000166:cytology; D018808:Transcription Factor AP-1 / Q000096:biosynthesis*; D014158:Transcription, Genetic / Q000187:drug effects; D014162:Transfection
D016328:NF-kappa B; D018808:Transcription Factor AP-1; D009532:Nickel