Deiodinases in thyroid tumorigenesis

in Endocrine-Related Cancer
Authors:
Maria Angela De StefanoM De Stefano, Public Health, Federico II University Hospital, Napoli, Italy

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Tommaso PorcelliT Porcelli, Public Health, Federico II University Hospital, Napoli, Italy

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Martin SchlumbergerM Schlumberger, Endocrine oncology and nuclear medicine, Gustave Roussy, Villejuif, France

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Domenico SalvatoreD Salvatore, Public Health, Federico II University Hospital, Napoli, Italy

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Correspondence: Domenico Salvatore, Email: domsalva@unina.it
Open access

The three deiodinase selenoenzymes are key regulators of intracellular thyroid hormone (TH) levels. The two TH-activating deiodinases (D1 and D2) are normally expressed in follicular thyroid cells and contribute to the overall TH production. During thyroid tumorigenesis, the deiodinase expression profile changes to customize intracellular TH levels to different requirements of cancer cells. Differentiated thyroid cancers overexpress the TH-inactivating D3, likely to reduce the TH signaling within the tumor. Strikingly, recent evidences suggest that during the late-stage of thyroid tumorigenesis D2 expression raises and this, together with a reduction in D3 expression levels, increases TH intracellular signaling in dedifferentiated thyroid cancers. These findings call into question the different function of TH on the various stages of thyroid cancers.

 

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