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Estrogen Receptor and Hormone Responsiveness of Medullary Thyroid Carcinoma Cells in Continuous Culture¹

Department of Medical Specialties, Section of Endocrinology, The University of Texas M. D. Anderson Hospital and Tumor Institute at Houston, Houston, Texas 77030

We have examined the estrogen responsiveness and estrogen receptor in medullary thyroid carcinoma using a model of an established human cell line, TT. TT cells bind [³H]estradiol with high affinity. Scatchard analysis reveals a single class of binding site with a concentration of 173 fmol/10⁶ cells and a dissociation constant of 2.1 x 10^-9 M, values which are comparable to those of a well established model cell line for estrogen responsiveness, MCF-7 human breast cancer cell line. Estradiol in physiological concentrations moderately stimulated TT cell proliferation, whereas in pharmacological concentrations it markedly inhibited cell growth. [³H]Thymidine incorporation into acid-insoluble material was also stimulated following a 5-day treatment with 5 x 10^-9 M estradiol. Tamoxifen at a concentration of 1 µM reduced cell proliferation by 43–48% after 5–7 days of treatment. The growth suppression induced by tamoxifen was reversed by addition of 10 nM estradiol. This is the first report of estrogen growth stimulation and tamoxifen growth inhibition of a tumor cell line derived from human medullary thyroid carcinoma.

¹ Research supported by NIH Grant CA27612-05 and by a grant from the Nancy Carmichael Gift Fund.

² To whom requests for reprints should be addressed.

Received 7/27/87. Revised 1/25/88. Accepted 2/22/88.