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Publication Detail

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

Authors: Huang, Yi; Davidson, Gerard; Li, Jingxia; Yan, Yan; Chen, Fei; Costa, Max; Chen, Lung Chi; Huang, Chuanshu

Published In Environ Health Perspect, (2002 Oct)

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.

PubMed ID: 12426142 Exiting the NIEHS site

MeSH Terms: Animals; Cell Culture Techniques; Fibroblasts; Humans; Inhalation Exposure*; Lung/cytology; Mice; NF-kappa B/biosynthesis*; Nickel/adverse effects*; Plasmids; Skin/cytology; Transcription Factor AP-1/biosynthesis*; Transcription, Genetic/drug effects; Transfection

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