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Science 18 October 1991:
Vol. 254. no. 5030, pp. 415 - 418
DOI: 10.1126/science.1925598
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Articles

Science, Vol 254, Issue 5030, 415-418
Copyright © 1991 by American Association for the Advancement of Science

articles

Targets for dioxin: genes for plasminogen activator inhibitor-2 and interleukin-1 beta

TR Sutter, K Guzman, KM Dold, and WF Greenlee

Chemical Industry Institute of Toxicology, Research Triangle Park, NC 27709.

Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD), a widespread environmental contaminant, may elicit its effects by altering gene expression in susceptible cells. Five TCDD-responsive complementary DNA clones were isolated from a human keratinocyte cell line. One of these clones encodes plasminogen activator inhibitor-2, a factor that influences growth and differentiation by regulating proteolysis of the extracellular matrix. Another encodes the cytokine interleukin-1 beta. Thus, TCDD alters the expression of growth regulatory genes and has effects similar to those of other tumor-promoting agents that affect both inflammation and differentiation.


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Dioxin-mediated tumor progression through activation of mitochondria-to-nucleus stress signaling.
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Carcinogen-induced histone alteration in normal human mammary epithelial cells.
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Ligand-Independent Regulation of Transforming Growth Factor {beta}1 Expression and Cell Cycle Progression by the Aryl Hydrocarbon Receptor.
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Interaction between the Aryl Hydrocarbon Receptor and Retinoic Acid Pathways Increases Matrix Metalloproteinase-1 Expression in Keratinocytes.
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Isolation and Characterization of the Human Cytochrome P450 CYP1B1 Gene.
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Human and Experimental Toxicology 15, 176-179
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Immune system impairment and hepatic fibrosis in mice lacking the dioxin-binding Ah receptor.
P Fernandez-Salguero, T Pineau, D. Hilbert, T McPhail, S. Lee, S Kimura, D. Nebert, S Rudikoff, J. Ward, and F. Gonzalez (1995)
Science 268, 722-726
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Toxicology goes molecular.
E Marshall (1993)
Science 259, 1394-1398
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