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 Google Scholar Google Scholar Articles by Yu, W. C. Y. Articles by Gao, Y. L. Search for Related Content PubMed PubMed Citation Articles by Yu, W. C. Y. Articles by Gao, Y. L.

Effects of 17ß-Estradiol on Progesterone Receptors and the Uptake of Thymidine in Human Breast Cancer Cell Line CAMA-1¹

Hormone Research Laboratory, Department of Obstetrics and Gynecology, University of Minnesota, Minneapolis, Minnesota 55455

Two sublines, CAMA-1R and CAMA-1N, were derived from the original CAMA-1 cells after continuous passages in our laboratory, 1R cells were supplemented in culture with estradiol and retained the properties of the original cell line, whereas 1N cells, not supplemented with estradiol, had a partial loss of estrogenic responsiveness. The doubling times for 1R and 1N cells were 2 and 2.4, respectively. These two sublines showed different effects on thymidine uptake after estradiol stimulation. Cells of 1R had a 2-fold greater thymidine incorporation than did the control without estradiol. In contrast, no difference of thymidine uptake was demonstrated in cells of 1N in the presence or absence of estradiol. Both cell lines contained cytoplasmic progesterone receptors with a K_d of 0.56 nM and a sedimentation coefficient of 6 to 7S on a 5 to 20% sucrose gradient. The progesterone receptor level in 1N was about 8-fold higher than in 1R cells. Both sublines exhibited a dose-dependent increase in progesterone receptor levels in response to estradiol with the maximal stimulation (8-fold increase) reached by using 5 nmol of estradiol. The rate of increase for estradiol-induced progesterone receptor appears to be the same for both sublines; a linear increase was demonstrated between Days 3 and 7 following plating. Our results show that estrogen regulation of thymidine uptake and progesterone receptor induction may be mediated through two separate mechanisms. Thus, following a chronically deficient supply of estradiol to 1N cells, there is apparent loss of responsiveness to estradiol-induced thymidine uptake, but the ability of these cells to respond to estradiol induction of progesterone receptor was retained.

¹ This investigation was supported by Grant 1RO1-CA 25998 and BRSG DC 3842 0685-5202, awarded by the National Cancer Institute, Department of Health, Education, and Welfare. A preliminary report of this work was presented (30).

² To whom requests for reprints should be addressed, at Box 395, Mayo Building, Department of Obstetrics and Gynecology, University of Minnesota, Minneapolis, Minn. 55455.

Received 4/ 9/81. Accepted 9/10/81.