Abstract
Human papillomavirus type 18 is a causative agent of epithelial cancers in the uterine cervix. We show here that estrogen and progesterone activate beta-galactosidase expression from the early promoter of this virus in the genital epithelia of transgenic mice. Ovariectomy caused suppression of transgene expression exclusively in vagina and cervix epithelia. Beta-galactosidase expression could be restored in ovariectomized females by administration of estrogen, alone or in combination with progesterone. Further, rescue of transgene expression was inhibited by the estrogen antagonist tamoxifen and the anti-progesterone RU486, suggesting that this was a specific effect.
(C)2002 Elsevier Science (USA).
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cervix Uteri / metabolism
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Epithelium / metabolism
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Estradiol / pharmacology*
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Estrous Cycle
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Female
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Gene Expression Regulation, Viral*
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Hormone Antagonists / pharmacology
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Mice
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Mice, Inbred C3H
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Mice, Inbred C57BL
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Mice, Transgenic
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Mifepristone / pharmacology
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Ovariectomy
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Papillomaviridae / drug effects
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Papillomaviridae / genetics*
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Pregnancy
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Progesterone / pharmacology*
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Promoter Regions, Genetic*
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Tamoxifen / pharmacology
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Transgenes
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Vagina / metabolism
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Viral Proteins / genetics
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Viral Proteins / metabolism
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beta-Galactosidase / genetics
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beta-Galactosidase / metabolism
Substances
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Hormone Antagonists
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Viral Proteins
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Tamoxifen
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Mifepristone
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Progesterone
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Estradiol
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beta-Galactosidase