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Fig. 27.3 ( continued )
inhibited estrogen-stimulated growth of MCF-7 cells; this effect was potentiated by the
antiestrogen drug hydroxytamoxifen. All- trans retinoic acid and 1,25(OH) 2 D 3 also
inhibit estrogen-induced transcription. It is possible that RA and 1,25(OH) 2 D 3 either
directly or indirectly inhibit the binding of estrogen to the estrogen receptor (ER) and, as
a consequence, ER fails to bind to the estrogen-responsive element. We have previously
shown that estrogen stimulation of the estrogen-responsive element results in upregulation
of the TauT gene in HCF-7 cells, but not in kidney cells (Han et al. 2006 ) .
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