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(American Journal of Pathology. 2004;165:25-34.)
© 2004 American Society for Investigative Pathology

Evidence for Transcriptional and Posttranscriptional Alterations of the Sodium/Iodide Symporter Expression in Hypofunctioning Benign and Malignant Thyroid Tumors

Séverine Trouttet-Masson*, Samia Selmi-Ruby*, Françoise Bernier-Valentin*, Valérie Porra*{dagger}, Nicole Berger-Dutrieux{ddagger}, Myriam Decaussin{ddagger}, Jean-Louis Peix{ddagger}, Agnès Perrin{ddagger}, Claire Bournaud{ddagger}, Jacques Orgiazzi{ddagger}, Françoise Borson-Chazot*{ddagger}, Brigitte Franc§ and Bernard Rousset*{dagger}

From UMR369 INSERM /Université Claude Bernard-Lyon 1 and Institut Fédératif de Recherche 62,* Faculté de Médecine Lyon-RTH Laennec, Lyon; Unité Fonctionnelle de Biologie Cellulaire,{dagger} Hôpital Edouard-Herriot, Lyon; Lyon Thyroid Tumor Bank Organization,{ddagger} Lyon; and INSERM U494 and Service d’Anatomie Patholologique,§ Hôpital Ambroise Paré, Boulogne-Billancourt, France

The uptake of iodide by epithelial thyroid cells requires the expression of a specific transporter, the Na+/I– symporter, NIS. Benign and malignant thyroid tumors of epithelial origin show a decrease up to a loss of iodide uptake activity. Previous studies of the human NIS (hNIS) gene expression in these tumors, based on the amplification of transcripts and/or immunohistochemical detection of the protein, have yielded divergent data; hNIS expression was found either increased or decreased. To get a new and integrated view of the alterations of hNIS expression in hypofunctioning thyroid tumors, we performed investigations of hNIS transcript and hNIS protein levels on the same tumors and paired normal tissue samples. HNIS, identified as a 75- to 80-kd species, was present in all normal tissue samples from euthyroid patients, but was undetectable, even at high membrane protein input, in all benign and malignant hypofunctioning thyroid tumors. By contrast, ~50% of tumors contained hNIS transcripts. This dissociation between transcript and protein levels was not found for the transcript and protein encoded by the PDS gene assayed in the same tumors. The hNIS transcript-positive tumors contained small amounts of low-molecular mass hNIS-immunoreactive species identified as nonglycosylated hNIS. Tumors containing the nonmature form of hNIS exhibited a predominant intracellular immunolabeling. In conclusion, our data show that benign and malignant hypofunctioning thyroid tumors either no longer express hNIS protein or express only a very low amount of nonglycosylated hNIS and indicate that the impairment of hNIS gene expression might result from alterations at both transcriptional and posttranscriptional levels.




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