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Carcinogenesis Advance Access published online on February 26, 2004
Carcinogenesis, doi:10.1093/carcin/bgh121
© 2004 by Oxford University Press
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© 2004 Oxford University Press

CANCER BIOLOGY

Indole-3-carbinol stimulates transcription of the interferon gamma receptor 1 gene and augments interferon responsiveness in human breast cancer cells

Urmi Chatterji 1, Jacques E. Riby 2, Taketoshi Taniguchi 3, Erik L. Bjeldanes 4, Leonard F. Bjeldanes 2, and Gary L. Firestone 1*

1 Dept. of Molecular and Cell Biology, University of California at Berkeley, Berkeley, CA 94720-3200; The Cancer Research Laboratory, University of California at Berkeley, Berkeley, CA 94720-3200
2 Department of Nutritional Sciences and Toxicology, University of California at Berkeley, Berkeley, CA 94720-3200
3 Laboratory of Molecular Biology, Medical Research Center, Kochi Medical School, Okoh, Nankoku, Kochi 783-8505, Japan
4 Incyte Genomics, Palo Alto, CA

* Corresponding author. E-mail: glfire{at}uclink4.berkeley.edu.

Received 24 September 2003 ; revised 15 January 2004 ; accepted 10 February 2004

Abstract

Indole-3-carbinol (I3C), a naturally occurring compound of Brassica vegetables, has promising anti-cancer properties and activates an anti-proliferative pathway that induces a G1 cell cycle arrest of human breast cancer cells. A microarray analysis of I3C treated versus untreated MCF-7 breast cancer cells revealed that I3C increased expression of the interferon gamma receptor 1 (IFN{gamma}R1). Western blot and RT-PCR analysis demonstrated that I3C strongly and rapidly stimulated IFN{gamma}R1 gene expression. Transfection of a series of 5' deletion constructs of the IFN{gamma}R1 reporter plasmids revealed that I3C significantly stimulates the promoter activity of the IFN{gamma}R1 and uncovered an I3C-responsive region between -540 bp and -240 bp of the IFN{gamma}R1 promoter. I3C stimulation of the IFN{gamma}R1 expression suggests that indole treatment should enhance interferon gamma responsiveness in breast cancer cells. A combination of I3C and IFN{gamma} synergistically activated STAT1 proteins by increasing phosphorylation at the Tyr-701 site. In addition, I3C and IFN{gamma} together more effectively induced a G1 cell cycle arrest and stimulated expression of the p21Waf1/Cip1 cell cycle inhibitor, compared to the effects of either agent alone. Our results suggest that one mechanism by which I3C mediates these anti-cancer effects is by stimulating expression of the IFN{gamma}R1 and augmenting the IFN{gamma} response in MCF-7 human breast cancer cells.


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