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Exp Clin Endocrinol Diabetes 1998; 106(4): 310-318
DOI: 10.1055/s-0029-1211991
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© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Regulation of the HGF-receptor c-met in the thyroid gland

K. M. Schulte, G. Antoch, M. Ellrichmann, M. Finken-Eigen* , K. Köhrer* , D. Simon, P. E. Goretzki, H. D. Röher
  • Dept. for General and Trauma Surgery, Heinrich Heine University, Düsseldorf, Germany
  • * Center for Biological and Medical Research, Heinrich Heine University, Düsseldorf, Germany
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Publication History

Publication Date:
14 July 2009 (online)

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Summary

HGF (hepatocyte growth factor) has been characterised as an important mitogen and motogen in many epithelial cells. The biological and clinical significance of HGF and its receptor c-met in the thyroid is currently under study. Overexpression of c-met is an important feature of papillary thyroid cancer. We developed a quantitative differential RT-PCR method in order to examine HGF-receptor regulation using RNA of about 50 cells per analysis. Experiments were performed in three spontaneously transformed follicular thyroid cancer (FTC) cell lines FTC-I 33, 236, and 238, 7 primary cultures derived from multinodular goitres, one from Graves disease and 1 from papillary thyroid cancer (PTC). TGF. alpha and to a minor degree HGF were shown to induce a marked up-regulation of the receptor whereas bovine TSH, NaT, dbcAMP or basic FGF had no apparent effect. We conclude that expression of the HGF-receptor is under control of paracrine growth factors activating tyrosine-kinase-dependent pathways. We could demonstrate a minor stimulation of thyroid cell proliferation by HGF in presence but not in absence of l0% fetal calf serum.

Key words

Hepatocyte growth factor - HGF - c-met - thyroid - neoplasia - proliferation - regulation - oncogene