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

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.

• Authors: Yi Huang, Gerard Davidson, Jingxia Li, Yan Yan, Fei Chen, Max Costa, Lung Chi Chen, Chuanshu Huang
• Journal: Environmental health perspectives (Environ Health Perspect) Vol. 110 Suppl 5 Pg. 835-9 (Oct 2002) ISSN: 0091-6765 [Print] United States
• PMID: 12426142 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• NF-kappa B
• Transcription Factor AP-1
• Nickel

Topics

• 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