| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Journal of Clinical Endocrinology & Metabolism, Vol 79, 806-813, Copyright © 1994 by Endocrine Society
ARTICLES |
T Holting, A Zielke, AE Siperstein, OH Clark and QY Duh
Department of Surgery, University of Heidelberg, Germany.
Invasion and metastasis may be caused by the escape of tumor cells from the negative control of growth factors. We analyzed the effects of transforming growth factor-beta 1 (TGF beta 1) on growth, migration, invasion, and adhesion in three follicular thyroid cancer cell lines (FTC133, primary; FTC236, lymph node metastasis; FTC238, lung metastasis) from one patient and in a papillary line (PTC-UC3). Cell growth was measured by dimethylthiazol-diphenyltetrazolium bromide assays, and migration (basal or epidermal growth factor stimulated) was determined by the ability of cells to penetrate 8-microns pore membranes that were covered with Matrigel for invasion assays. Moreover, we studied tumor cell adhesion to collagen type IV, fibronectin, and laminin. TGF beta 1 inhibited growth in FTC (FTC133, by 31%; FTC236, 15%; FTC238, 17%; P < 0.008), but not in PTC. Migration was inhibited in all cell lines. TGF beta 1 inhibited epidermal growth factor-stimulated migration of FTC133 by 43% vs. 29% without epidermal growth factor (P < 0.03). TGF beta 1 also inhibited invasion (FTC133, 32%; FTC236, 18%; FTC238, 16%; PTC-UC3, 32%; P < 0.02). All cell lines adhered preferably to collagen type IV and fibronectin. TGF beta 1 enhanced adhesion. Again, these effects were less pronounced in the FTC metastases. In conclusion, TGF beta 1 inhibits the growth, migration, and invasion of thyroid cancer cells in vitro. It enhances adhesion to components of the extracellular matrix. Metastatic thyroid tumors may be less responsive to the negative regulation of TGF beta 1.
This article has been cited by other articles:
 |
|
 |
|
  S. E. Matsuo, S. G. Leoni, A. Colquhoun, and E. T. Kimura Transforming growth factor-{beta}1 and activin A generate antiproliferative signaling in thyroid cancer cells. J. Endocrinol., July 1, 2006; 190(1): 141 - 150. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Hoffmann, L. C. Hofbauer, V. Scharrenbach, A. Wunderlich, I. Hassan, S. Lingelbach, and A. Zielke Thyrotropin (TSH)-Induced Production of Vascular Endothelial Growth Factor in Thyroid Cancer Cells in Vitro: Evaluation of TSH Signal Transduction and of Angiogenesis-Stimulating Growth Factors J. Clin. Endocrinol. Metab., December 1, 2004; 89(12): 6139 - 6145. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-C. Kang, M. Ohmori, N. Harii, T. Endo, and T. Onaya Pax-8 Is Essential for Regulation of the Thyroglobulin Gene by Transforming Growth Factor-{beta}1 Endocrinology, January 1, 2001; 142(1): 267 - 275. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Napolitano, V. Montani, C. Giuliani, S. Di Vincenzo, I. Bucci, V. Todisco, G. Laglia, A. Coppa, D. S. Singer, M. Nakazato, et al. Transforming Growth Factor-{beta}1 Down-Regulation of Major Histocompatibility Complex Class I in Thyrocytes: Coordinate Regulation Of Two Separate Elements by Thyroid-Specific as Well as Ubiquitous Transcription Factors Mol. Endocrinol., April 1, 2000; 14(4): 486 - 505. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
