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Carcinogenesis Advance Access originally published online on July 28, 2005
Carcinogenesis 2006 27(1):131-136; doi:10.1093/carcin/bgi199
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Carcinogenesis vol.27 no.1 © Oxford University Press 2005; all rights reserved.

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

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

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

* To whom correspondence should be addressed at: Department of Microbiology, National Taiwan University College of Medicine, No. 1, Sec. 1, Jen-Ai Road, Taipei 100, Taiwan. Tel: +886 2 2312 3456 ext. 8282; Fax: +886 2 23915293; Email: scteng{at}ha.mc.ntu.edu.tw

The phytochemical dibenzoylmethane (DBM) has been shown to inhibit 7,12-dimethylbenz[a]anthracene induced mammary tumorigenesis in Sencar mice. However, the molecular basis of this activity is still elusive. In the present study, we demonstrated that DBM inhibits estradiol (E2)-induced incorporation of bromodeoxyuridine 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 E2. 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 assay demonstrated that DBM acts as a pure antagonist by attenuating the binding of estrogen receptor to the estrogen response elements 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 antiestrogenic drugs.


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