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Nuclear Thyroid Hormone Receptors in a Human Breast Cancer Cell Line¹

Department of Medicine, The University of Texas Health Science Center, San Antonio, Texas 78284

Proliferation of a human metastatic breast cancer cell line derived at the Michigan Cancer Foundation (MCF-7) was stimulated significantly (p < 0.05) by the addition of L-3,3'-5-triiodothyronine (T3) to the culture medium. An optimal effect was observed near 5 x 10^-10 M.

Thyroid hormone receptor was assayed by comparing the radioactive [¹²⁵I]T3 incorporated by MCF-7 cells incubated in culture with and without unlabeled competitor. Bound [¹²⁵I]T3 in the nuclei was determined directly by counting Triton X-100-purified nuclear pellets. Saturable or competible binding was not demonstrable for whole cells.

MCF-7 nuclei contain a relatively small number of specific T3-binding sites (20 fmol/100 µg DNA, or 1200 sites/cell) with high affinity (K_d = 1 x 10^-10 M). The relative effectiveness of unlabeled structural analogs to T3 as competitors for [¹²⁵I]T3 binding was: T3 = 3,5-diiodo-3'-isopropyl-L-thyronine > D-3,3',5-triiodothyronine > L-thyroxine = 3,3',5,5'-tetraiodo-L-thyroacetic acid > reverse 3,3',5'-triiodo-L-thyronine. The mono- and diiodotyrosines, bovine insulin, ovine prolactin, 17ß-estradiol, prostaglandin F₂, indomethacin, and propylthiouracil did not compete for binding sites. Nuclear receptor levels were not altered by treatment of MCF-7 cells with these compounds or with T3 itself. Receptor levels also did not fluctuate with the growth phase.

Our data establish the presence of receptors for thyroid hormone in nuclei of cells derived from a human breast cancer.

¹ This research was supported in part by the National Cancer Institute (Grants CA-11378, CB23862, and CA 09042), American Cancer Society Grant BC 23, and the Robert A. Welch Foundation.

² To whom requests for reprints should be addressed.

Received 6/27/77. Accepted 7/25/78.