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Vol. 56, Issue 1, 31-38, July 1999
Division of Neurology, University Department of Medicine,
University of Hong Kong, Queen Mary Hospital, Hong Kong (X.T., S.L.H.);
and Department of Medicine, University of Birmingham, Queen Elizabeth
Hospital, United Kingdom (D.R.)
Catechol-O-methyltransferase (COMT, EC 2.1.1.6) is a
ubiquitous enzyme that is crucial to the metabolism of carcinogenic catechols and catecholamines. Regulation of human COMT gene expression may be important in the pathophysiology of various human disorders including estrogen-induced cancers, Parkinson's disease, depression, and hypertension. The gender difference in human COMT activity and
variations in rat COMT activity during the estrous cycle led us to
explore whether estrogen can regulate human COMT gene transcription. Our Northern analyses showed that physiological concentrations of
17-
-estradiol (10
9-107 M) could
decrease human 1.3-kilobase COMT mRNA levels in MCF-7 cells in a time-
and dose-dependent manner through an estrogen receptor-dependent
mechanism. Two DNA fragments immediately 5' to the published human COMT
gene proximal and distal promoters were cloned. Sequence analyses
revealed several half-palindromic estrogen response elements and
CCAAT/enhancer binding protein sites. By cotransfecting COMT
promoter-chloramphenicol acetyltransferase reporter genes with human
estrogen receptor cDNA and pSV--galactosidase plasmids into COS-7
cells, we showed that 17--estradiol could down-regulate
chloramphenicol acetyltransferase activities, and COMT promoter
activities dose-dependently. Functional deletion analyses of COMT
promoters also showed that this estrogenic effect was mediated by a 280 base pair fragment with two putative half-palindromic estrogen response
elements in the proximal promoter and a 323-base pair fragment with two
putative CCAAT/enhancer binding protein sites in the distal promoter.
Our findings provide the first evidence and molecular mechanism for
estrogen to inhibit COMT gene transcription, which may shed new insight
into the role of estrogen in the pathophysiology of different human disorders.
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