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. 2002 Oct;110(Suppl 5):835–839. doi: 10.1289/ehp.02110s5835

Activation of nuclear factor-kappaB and not activator protein-1 in cellular response to nickel compounds.

Yi Huang 1, Gerard Davidson 1, Jingxia Li 1, Yan Yan 1, Fei Chen 1, Max Costa 1, Lung Chi Chen 1, Chuanshu Huang 1
PMCID: PMC1241256  PMID: 12426142

Abstract

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.

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Selected References

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