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Journal of Thyroid Research
Volume 2011, Article ID 431718, 13 pages
Review Article

EGF and TGF- 𝛽 1 Effects on Thyroid Function

1Department of Oncology and Experimental Medicine, University “G. d'Annunzio” Chieti-Pescara, 66013 Chieti, Italy
2Center of Excellence on Aging, Ce.S.I., “G. d'Annunzio” University Foundation, 66013 Chieti, Italy
3Department of Experimental Medicine and Department of Radiological Sciences Oncology and Anatomical Pathology, Sapienza University of Rome, Viale Regina Elena, 324, 00161 Rome, Italy

Received 14 January 2011; Accepted 22 March 2011

Academic Editor: Guillermo Juvenal

Copyright © 2011 Gabriella Mincione et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Normal epithelial thyroid cells in culture are inhibited by TGF- 𝛽 1. Instead, transformed thyroid cell lines are frequently resistant to its growth inhibitory effect. Loss of TGF- 𝛽 responsiveness could be due to a reduced expression of TGF- 𝛽 receptors, as shown in transformed rat thyroid cell lines and in human thyroid tumors, or to alterations of other genes controlling TGF- 𝛽 signal transduction pathway. However, in thyroid neoplasia, a complex pattern of alterations occurring during transformation and progression has been identified. Functionally, TGF- 𝛽 1 acts as a tumor suppressor in the early stage of transformation or as a tumor promoter in advanced cancer. This peculiar pleiotropic behaviour of TGF- 𝛽 may result from cross-talk with signalling pathways mediated by other growth factors, among which EGF-like ligands play an important role. This paper reports evidences on TGF- 𝛽 1 and EGF systems in thyroid tumors and on the cross-talk between these growth factors in thyroid cancer.