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Tamoxifen Stimulates Human Papillomavirus Type 16 Gene Expression and Cell Proliferation in a Cervical Cancer Cell Line¹

Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan, Republic of China

³ To whom requests for reprints should be addressed.

The widely adopted use of tamoxifen as a chemotherapeutic agent is primarily based on its inhibition of cancer cell growth. However, we report that tamoxifen at low concentrations (10^–9 and 10^–11 M) causes stimulation of cell proliferation in a cervical cancer cell line, SFR. The facts that SFR cells do not contain estrogen receptors and are estrogen nonresponsive imply the existence of an antiestrogen-specific binding protein and suggest that the effect of tamoxifen is possibly mediated through a pathway other than estrogen receptors. Tamoxifen at low concentrations stimulated human papillomavirus type 16 (HPV-16) gene transcription and E7 protein production. Levels of HPV-16 mRNA and E7 protein reached a peak at approximately 2–4 h after tamoxifen treatment, persisted for several hours, and subsequently decreased to their prestimulation levels by about 24 h after treatment. Our results indicate for the first time that tamoxifen stimulates cell proliferation of cervical cancer cells, and we suggest that the enhanced HPV-16 mRNA and E7 protein levels are probably responsible.

¹ Supported in part by National Science Council Grant 81-0412-B-001-04 to W. C. Y. Y.

² National University Preparatory School for Overseas Chinese Students.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 6/12/92. Accepted 10/ 6/92.

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