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Carcinogenesis Advance Access published online on August 5, 2004
Carcinogenesis, doi:10.1093/carcin/bgh243
© 2004 by Oxford University Press
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Received May 21, 2004
Revised July 14, 2004
Accepted July 18, 2004

CARCINOGENESIS

Tobacco smoke induces CYP1B1 in the aerodigestive tract

Jeffrey L. Port 1, Kentaro Yamaguchi 2, Baoheng Du 2, Mariana De Lorenzo 2, Mindy Chang 2, Paul M. Heerdt 3, Levy Kopelovich 4, Craig B. Marcus 5, Nasser K. Altorki 1, Kotha Subbaramaiah 6, Andrew J. Dannenberg 6*

1 Department of Cardiothoracic Surgery, Weill Medical College of Cornell University, New York, N.Y. 10021
2 Department of Medicine, Weill Medical College of Cornell University, New York, N.Y. 10021
3 Department of Anesthesiology, Weill Medical College of Cornell University, New York, N.Y. 10021
4 DCP, National Cancer Institute, Bethesda, MD 20892
5 University of New Mexico Health Sciences Center, College of Pharmacy, Albuquerque, N.M. 87131
6 Department of Medicine, Weill Medical College of Cornell University, New York, N.Y. 10021; Strang Cancer Prevention Center, New York, N.Y. 10021

* To whom correspondence should be addressed. E-mail: ajdannen{at}med.cornell.edu.


  Abstract

Several members of the P450 family including cytochrome P450 1B1 (CYP1B1) can convert tobacco smoke (TS) procarcinogens including benzo[a]pyrene (B[a]P) to carcinogenic intermediates. In this study, we investigated the effects of TS condensate and B[a]P on the expression of CYP1B1 in vitro and in vivo. CYP1B1 mRNA and protein were induced by both TS condensate and B[a]P in cell lines derived from the human aerodigestive tract. Treatment with TS condensate stimulated binding of the AhR to an oligonucleotide containing a canonical XRE site and induced XRE-luciferase activity. These findings are consistent with prior evidence that PAHs, known ligands of the AhR, stimulate CYP1B1 transcription by an XRE-dependent mechanism. To determine whether these in vitro findings translated in vivo, both murine and human studies were carried out. Short-term exposure to TS induced CYP1B1 in the tongue, esophagus, lung and colon of experimental mice. In contrast, CYP1B1 was not induced by TS in the aorta of these mice. Levels of CYP1B1 mRNA were also elevated in the bronchial mucosa of human tobacco smokers vs. never smokers (P<0.05). Taken together, these results support a role for CYP1B1 in TS-induced carcinogenesis in the aerodigestive tract.


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