This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bezwoda, W. R. Articles by Meyer, K. Search for Related Content PubMed PubMed Citation Articles by Bezwoda, W. R. Articles by Meyer, K.

Effect of -Interferon, 17ß-Estradiol, and Tamoxifen on Estrogen Receptor Concentration and Cell Cycle Kinetics of MCF 7 Cells¹

Department of Medicine, Division of Haematology/Oncology, University of the Witwatersrand, Parktown 2193, Johannesburg, South Africa

The interaction of -interferon, 17ß-estradiol, and tamoxifen on estrogen receptor content, growth fraction, proliferative rate, and total protein synthesis of MCF 7 cells was investigated under culture conditions (minus phenol red and at low concentrations of "stripped" fetal calf serum) allowing for direct stimulation of proliferation by estrogens. Exposure to estradiol alone resulted in a decrease of estrogen receptor content as measured by immunoassay, an increase of the proportion of cells in S phase, and increases in cell proliferation as well as total protein synthesis. -Interferon treatment resulted in cell cycle arrest with reduced proliferation, an increase of estrogen receptor content, but a decrease in the rate of total protein synthesis. Pretreatment with -interferon inhibited the estrogen induced stimulation of cell growth as well as the associated decrease of estrogen receptor content. Tamoxifen treatment resulted in decreased cell proliferation and decrease of estrogen receptor content and of total protein synthesis. These results suggest that the estrogen receptor concentration of MCF 7 cells is growth fraction related. Pretreatment with -interferon enhanced the inhibitory effect of tamoxifen on cell proliferation while preventing the tamoxifen induced reduction of estrogen receptor content. The synergistic effect of -interferon and tamoxifen are most marked following 72 h pretreatment with interferon, when the maximum interferon induced increase of estrogen receptor concentration is evident. The mechanism is thus due probably to an increase of cellular receptor as a ligand for tamoxifen binding and suggests a possible role for the clinical use of interferons combined with tamoxifen.

¹ Supported by Grants from the National Cancer Association (South Africa) and Bekker Trust Foundation.

² To whom requests for reprints should be addressed, at Department of Medicine, University of the Witwatersrand, Medical School, 7 York Road, Parktown 2193, Johannesburg, South Africa.

Received 10/ 2/89. Revised 4/18/90.

This article has been cited by other articles:

				J. Lu, A. Pierron, and K. Ravid An Adenosine Analogue, IB-MECA, Down-Regulates Estrogen Receptor {alpha} and Suppresses Human Breast Cancer Cell Proliferation Cancer Res., October 1, 2003; 63(19): 6413 - 6423. [Abstract] [Full Text] [PDF]