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Issue 2, 2003
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GeneChip analysis of signaling pathways effected by nickel

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Abstract

The carcinogenicity of nickel compounds has been shown in numerous epidemiological and animal studies. Carcinogenesis is generally considered as a multistep accumulation of genetic alterations. Nickel, however, being highly carcinogenic is only a weak mutagen. We hypothesize that nickel may act by modulating signaling pathways, and subsequently by reprogramming transcription factors. Insoluble nickel is considered to be more carcinogenic than soluble. In this study using GeneChip technology we compared changes in gene expression caused by soluble and insoluble nickel compounds. We found that both soluble and insoluble nickel compounds induce similar signaling pathways following 20 h of in vitro exposure. For example, both nickel compounds activated a number of transcription factors including hypoxia-inducible factor I (HIF-1) and p53. The induction of these important transcription factors exerts potent selective pressure leading to cell transformation. The obtained data are in agreement with our previous observations that acute nickel exposure activates HIF-1 and p53 transcription factors and in nickel-transformed cells, the ratio of HIF-I activity to p53 activity was shifted towards high HIF-I activity. The activation of the same signaling pathways by soluble and insoluble nickel compounds suggested that both nickel compounds have similar carcinogenic potential in vitro.

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Publication details

The article was received on 18 Oct 2002, accepted on 17 Feb 2003 and first published on 27 Feb 2003


Article type: Paper
DOI: 10.1039/B210262P
Citation: J. Environ. Monit., 2003,5, 206-209

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    GeneChip analysis of signaling pathways effected by nickel

    K. Salnikow, T. Davidson, T. Kluz, H. Chen, D. Zhou and M. Costa, J. Environ. Monit., 2003, 5, 206
    DOI: 10.1039/B210262P

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