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[Cancer Research 60, 38-41, January 1, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

Carcinogenic Nickel Induces Genes Involved with Hypoxic Stress1

Konstantin Salnikow2, Mikhail V. Blagosklonny, Heather Ryan, Randall Johnson and Max Costa

Nelson Institute of Environmental Medicine, and Kaplan Comprehensive Cancer Center, New York University School of Medicine, New York, New York 10016 [K. S., M. C.]; Medicine Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892 [M. B.]; and Department of Biology, Center for Molecular Genetics, University of California, San Diego, La Jolla, California 92093-0366 [H. R., R. J.]

Carcinogenic nickel compounds alter the program of gene expression in normal cells and induce a pattern of gene expression similar to that found in nickel-induced cancers. Here we have demonstrated that nickel exposure induced hypoxic signaling pathways by inducing hypoxia-inducible transcription factor-1 (HIF-1), which mediated the induction of genes required by cells to survive hypoxia. We also show that a new gene, Cap43, is dependent upon HIF-1 because only HIF-1-proficient cells induced Cap43 when exposed to either hypoxia or nickel. We also show that glyceraldehyde-3-phosphate dehydrogenase, a gene induced by hypoxia through HIF-1, was similar to Cap43 in that it required HIF-1-proficient cells to be induced by either nickel or hypoxia. These data demonstrate that nickel exposure turns on signaling for hypoxic stress, which may be important in its carcinogenesis.




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