Journal Article

Inhibition of estradiol-induced mammary proliferation by dibenzoylmethane through the E<sub>2</sub>–ER–ERE-dependent pathway

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

in Carcinogenesis

Volume 27, issue 1, pages 131-136
Published in print January 2005 | ISSN: 0143-3334
Published online July 2005 | e-ISSN: 1460-2180 | DOI:
Inhibition of estradiol-induced mammary proliferation by dibenzoylmethane through the E2–ER–ERE-dependent pathway

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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.

Keywords: BrdU, bromodeoxyuridine; ChIP, chromatin immunoprecipitation; DBM, dibenzoylmethane; DMBA, 7,12-dimethylbenz[a]anthracene; E2, estradiol; ER, estrogen receptor, EREs, estrogen response elements; i.p., intraperitoneal

Journal Article.  4899 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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