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Carcinogenesis Advance Access published online on July 28, 2005
Carcinogenesis, doi:10.1093/carcin/bgi199
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oupjournals.org
Received May 25, 2005
Revised July 21, 2005
Accepted July 22, 2005

CARCINOGENESIS

Inhibition of estradiol-induced mammary proliferation by dibenzoylmethane through the E2-ER-ERE-dependent pathway

Chuan-Chuan Lin 1, Yun-Luen Tsai 2, Mou-Tuan Huang 3, Yao-Ping Lu 3, Chi-Tang Ho 4, Shun-Fu Tseng 2, and Shu-Chun Teng 5*

1 Department of Food Science, China Institute of Technology, Taipei, 115, Taiwan
2 Department of Microbiology, College of Medicine, National Taiwan University, Taipei, 100, Taiwan
3 Laboratory for Cancer Research, School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854-8020, USA
4 Department of Food Science and Center for Advanced Food Technology, Rutgers University, New Brunswick, NJ 08901-8520, USA
5 Department of Microbiology, College of Medicine, National Taiwan University, Taipei, 100, Taiwan; Institute of Internal Medicine, National Taiwan University Hospital, Taipei, 100, Taiwan

* To whom correspondence should be addressed.
Shu-Chun Teng, E-mail: scteng{at}ha.mc.ntu.edu.tw


  Abstract

The phytochemical dibenzoylmethane (DBM) has been shown to inhibit DMBA-induced mammary tumorigenesis in Sencar mice. However, the molecular basis of this activity is still elusive. Here, we demonstrated that DBM inhibits estradiol (E2)-induced incorporation of bromodeoxyuridine (BrdU) into mammary DNA in immature female Sencar mice by 52%, when 10 µmol of DBM was intraperitoneally injected into mice prior to the injection of estradiol. Examination of the influence of DBM on the expressions of E2-ERE-dependent oncogenes in MCF-7 cells indicated that DBM inhibits the E2-induced cell growth as well as the expressions of four oncogenes, telomerase, c-myc, Ha-ras and bcl-2. Further mechanistic study using chromatin immunoprecipitation (ChIP) assay demonstrated that DBM acts as a pure antagonist by attenuating the binding of ER to the EREs in the regulatory regions of c-myc, hTERT and bcl-2 genes in vivo. Taken together, our results strongly suggest that DBM plays an inhibitory role in E2-induced proliferations, which establishes DBM as a model molecule for studying the anti-estrogenic drugs.

Keywords: dibenzoylmethane; estradiol; estrogen receptor; estrogen response element; oncogene.
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