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*Compound via MeSH
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Medline Plus Health Information
*Thyroid Cancer
The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 8 2633-2638
Copyright © 1997 by The Endocrine Society

Endocrinological Oncology

Growth Inhibition of New Human Thyroid Carcinoma Cell Lines by Activation of Adenylate Cyclase through the ß-Adrenergic Receptor1

Kazuyasu Ohta, Xuan-Ping Pang, Loretta Berg and Jerome M. Hershman

Endocrine Research Laboratory, West Los Angeles Veterans Affairs Medical Center, and University of California School of Medicine, Los Angeles, California 90073

Address all correspondence and requests for reprints to: Jerome M. Hershman, M.D., Endocrinology Division 111D, West Los Angeles Veterans Administration Medical Center, Los Angeles, California 90073. E-mail: jhershmn{at}ucla.edu

In normal thyroid cells, the TSH-adenylate cyclase system plays a pivotal role in controlling growth and differentiation. However, the role of this system in the growth of thyroid carcinoma is not well understood. To investigate this subject, we have established four new human thyroid carcinoma cell lines, designated BHP 2–7, 7–13, 10–3, and 18–21, from different patients. Northern gel analysis revealed that all of these cell lines expressed Pax-8 messenger ribonucleic acid; additionally, only BHP 18–21 cells expressed TTF-1 messenger ribonucleic acid. These cells were treated with various concentrations of 8-bromo-cAMP, forskolin, TSH, and adrenergic receptor agonist (norepinephrine, epinephrine, and isoproterenol). Cell proliferation was assessed by [3H]thymidine incorporation and cell number. In these human thyroid carcinoma cell lines, the addition of 8-bromo-cAMP reduced [3H]thymidine incorporation at a concentration of 10 µmol/L. Forskolin (0.1–10 µmol/L) significantly induced cAMP accumulation, decreased [3H]thymidine incorporation, and reduced cell number in a dose-dependent manner. Conversely, TSH (0.01–1 mU/mL) did not affect the accumulation of cAMP or cell growth. We found that adrenergic receptor agonists induced the accumulation of cAMP and inhibited cell growth. The rank of potency was isoproterenol > epinephrine >> norepinephrine. The binding studies of [3H]CGP-12177, a specific ß-adrenergic agonist, revealed that these new thyroid carcinoma cells had ß-adrenergic receptors. These results indicate that cAMP inhibits the growth of some human thyroid carcinoma cells, and that cAMP production is regulated through ß-adrenergic receptor-mediated pathways, but not through TSH receptor-mediated pathways.




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