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 Soto, A. M. Articles by Sonnenschein, C. Search for Related Content PubMed PubMed Citation Articles by Soto, A. M. Articles by Sonnenschein, C.

Control of Cell Proliferation: Evidence for Negative Control on Estrogen-sensitive T47D Human Breast Cancer Cells¹

Department of Anatomy and Cellular Biology, Tufts University School of Medicine, Boston, Massachusetts 02111 [A. M. S., C. S.], and Department of Obstetrics and Gynecology, University of California School of Medicine, San Francisco, California 94143 [J. T. M., P. K. S.]

The human breast tumor cloned cell lines T47D-A8 and All are estrogen dependent for cell proliferation in the nude mouse model. In contrast, these cells multiplied at similar rates when grown in serum-free cultures, regardless of the presence of 17ß-estradiol (3 x 10^-11 to 3 x 10^-8 M estradiol). Addition of 10% charcoal-dextran stripped human female serum to the culture medium resulted in a marked inhibition of cell proliferation. The addition of 3 x 10^-11 M estradiol overcame the inhibitory effect of serum. Similar results were obtained with the human breast tumor C₇MCF7 cell line. Both cell lines contain similar estrophilin levels. The K_d of the estrophilin-estradiol complex was 0.39 x 10^-10 M for C₇MCF7 cells and 4.4 x 10^-10 M for T47D-A11 cells. Maximal cell yields were achieved at 5 x 10^-12 M free estradiol levels in 10% charcoaldextran stripped serum supplemented medium. These data are compatible with the following interpretation: (a) estradiol-sensitive cells are inhibited from proliferating by a serum-borne factor; and (b) estradiol neutralizes this inhibitory effect. This mechanism seems not to be mediated by estradiol binding to the cellular estrophilins because (a) the free estradiol levels needed for maximal response are significantly lower than the estrophilin K_ds, and (b) maximal proliferation rates occur at similar estradiol concentrations for these three cell lines, regardless of the binding properties of their estrophilins.

¹ This work was supported in part by USPHS Grant CA 13410 awarded by the National Cancer Institute.

² To whom requests for reprints should be addressed.

Received 4/16/85. Revised 8/28/85. Revised 12/10/85. Accepted 1/21/86.

This article has been cited by other articles:

				T Eliades, V Gioni, D Kletsas, A. Athanasiou, and G Eliades Oestrogenicity of orthodontic adhesive resins Eur J Orthod, August 1, 2007; 29(4): 404 - 407. [Abstract] [Full Text] [PDF]

				J. P Wiebe Progesterone metabolites in breast cancer. Endocr. Relat. Cancer, September 1, 2006; 13(3): 717 - 738. [Abstract] [Full Text] [PDF]