par Laatikainen, Lilja E;Castellone, Maria D;Hebrant, Aline 
;Hoste, Candice ;Cantisani, Maria C;Laurila, Juha P;Salvatore, Giuliana;Salerno, Paolo;Basolo, Fulvio;Näsman, Johnny;Dumont, Jacques Emile ;Santoro, Massimo;Laukkanen, Mikko O
Référence Endocrine-related cancer, 17, 3, page (785-796)
Publication Publié, 2010-09
;Hoste, Candice ;Cantisani, Maria C;Laurila, Juha P;Salvatore, Giuliana;Salerno, Paolo;Basolo, Fulvio;Näsman, Johnny;Dumont, Jacques Emile ;Santoro, Massimo;Laukkanen, Mikko ORéférence Endocrine-related cancer, 17, 3, page (785-796)
Publication Publié, 2010-09
Article révisé par les pairs
| Résumé : | Reactive oxygen species, specifically hydrogen peroxide (H(2)O(2)), have a significant role in hormone production in thyroid tissue. Although recent studies have demonstrated that dual oxidases are responsible for the H(2)O(2) synthesis needed in thyroid hormone production, our data suggest a pivotal role for superoxide dismutase 3 (SOD3) as a major H(2)O(2)-producing enzyme. According to our results, Sod3 is highly expressed in normal thyroid, and becomes even more abundant in rat goiter models. We showed TSH-stimulated expression of Sod3 via phospholipase C-Ca(2+) and cAMP-protein kinase A, a pathway that might be disrupted in thyroid cancer. In line with this finding, we demonstrated an oncogene-dependent decrease in Sod3 mRNA expression synthesis in thyroid cancer cell models that corresponded to a similar decrease in clinical patient samples, suggesting that SOD3 could be used as a differentiation marker in thyroid cancer. Finally, the functional analysis in thyroid models indicated a moderate role for SOD3 in regulating normal thyroid cell proliferation being in line with our previous observations. |
