Journal
JOURNAL OF MOLECULAR ENDOCRINOLOGY
Volume 26, Issue 1, Pages 31-42Publisher
BIOSCIENTIFICA LTD
DOI: 10.1677/jme.0.0260031
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- NIEHS NIH HHS [ES04176, ES09106] Funding Source: Medline
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Heat shock protein 27 (Hsp 27) is expressed in mammary tumors and may play a role in tumor growth and response to anti-neoplastic drug therapy. 17 beta -Estradiol (E-2) induces Hsp 27 mRNA levels in MCF-7 human breast cancer cells, and we have investigated the comparative inhibitory mechanisms using the aryl hydrocarbon receptor (AhR) agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the direct-acting antiestrogen ICI 164,384. TCDD inhibited E-2-induced Hsp 27 gene expression and analysis of the Hsp 27 gene promoter showed that the inhibitory response was associated with AhR interactions with a pentanucleotide motif at - 3 to + 2 in the promoter that corresponded to the core sequence of a dioxin responsive element. In contrast, ICI 164,384 induced Hsp 27 gene expression and reporter gene activity in MCF-7 cells and this represents one of the few examples of the estrogen receptor-alpha (ER alpha) agonist activity of the 'pure' antiestrogen ICI 164,384.
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