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Endocrine Abstracts (2016) 41 OC14.3 | DOI: 10.1530/endoabs.41.OC14.3


1Endocrine Unit, Fondazione IRCCS Ca’ Granda, Milan, Italy; 2Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy; 3Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy; 4Endocrine Surgery Unit, Fondazione IRCCS Ca’ Granda, Milan, Italy.

Abstract: During hormonogenesis, thyroid cells are physiologically exposed to high levels of reactive oxygen species (ROS) which could either be involved in the pathogenesis of thyroid cancer or exert a cytotoxic effect. We analyzed the oxidative status of papillary thyroid cancer (PTC) either directly, by measuring H2O2 generation by NADPH oxidases (NOXs), and indirectly, by evaluating the antioxidant activity of glutathione peroxidase (GPX), which neutralizes H2O2 excess, and lipid peroxidation (LP). Moreover, since TERT exhibits a stress protection activity upon its translocation to the mitochondria, we investigated its subcellular localization in PTC.

A significantly higher calcium-dependent and independent H2O2 generation activity was found in tumors with respect to normal tissues. Interestingly, BRAF/RAS mutated tumors had a H2O2 production higher than wild-type tumors, and a trend towards a higher H2O2 generation activity was found in tumors from females compared to males. The GPX activity was found to be higher in PTCs with respect to normal tissues, and was significantly increased in tumors from young than from older patients, while no differences were found in lipid peroxidation. GPX activity. Moreover, we demonstrated for the first time the mitochondrial localization of TERT in PTC, suggesting that the elevated ROS levels associated with TC could be responsible for the shuttling of TERT from the nucleus to the mitochondria.

In conclusion, present data demonstrate that PTCs are exposed to elevated ROS, with a potential cytotoxic effect. Nevertheless, the increase of GPX activity and the mitochondrial localization of TERT seem to be able to compensate the damage derived from the excessive ROS exposure, supporting the neoplastic process.

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