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Arquivos Brasileiros de Endocrinologia & Metabologia

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Abstract

KIMURA, Edna T.; MATSUO, Sílvia E.  and  RICARTE-FILHO, Júlio Cézar. TGFb, activin and SMAD signalling in thyroid cancer. Arq Bras Endocrinol Metab [online]. 2007, vol.51, n.5, pp. 683-689. ISSN 0004-2730.  http://dx.doi.org/10.1590/S0004-27302007000500005.

TGFb and activin are members of the TGFb superfamily and play a wide role in development, proliferation and apoptosis. These growth factors exert their biological effects by binding to the type I and II membrane receptors to transduce their signalling through the nucleus by phosphorylation of R-SMADs (SMAD 2/3) and co-SMADs (Smad 4). The proper control of TGFb/activin pathway is negatively regulated by inhibitory SMAD (SMAD7) and by E3 ubiquitination enzymes (Smurfs). Physiologically, TGFb and activin act as potent growth inhibitors in thyroid follicular cell. Thus, alterations in the receptors and components of SMAD signalling pathway are associated with several types of tumors. Since TGFb and activin generate their intracellular signalling through the same components of the SMAD pathway, the unbalance of this pathway impairs both of anti-mitogenic signals in the cell. This review addresses aspects of the molecular mechanisms in the understanding of resistance to the growth inhibitory effects of TGFb and activin due to the disequilibrium in the SMAD inhibitory pathway in thyroid neoplasia.

Keywords : TGFb; Activin; Thyroid cancer; SMAD signalling; Smurf; Tumor progression.

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