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Functional Expression of Sodium Iodide Symporter (NIS) in Human Breast Cancer Tissue

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Abstract

Sodium iodide symporter (NIS) is a molecule involved in active accumulation of iodine in thyroid gland for the biosynthesis of thyroid hormone. Its expression has also been demonstrated in extra-thyroidal tissues including lactating mice mammary gland and also in human breast cancers. Iodide transport in thyroid cells through NIS is the basis for using radioiodine for diagnosis and treatment of differentiated thyroid carcinoma. The similar approach may prove beneficial for the diagnosis and treatment of breast cancer if iodine uptake, its retention and NIS expression can be shown unequivocally in malignant tumors. The aim of the present study was to investigate NIS expression, in vivo iodine transport ability and fate of iodine in human breast tumors. Women (age 33–58 years) with infiltrating duct carcinoma confirmed by FNAC and subsequent histopathology were the subject of this study. Expression of NIS RNA and protein was confirmed by RNAase protection assay, western blot and immunohistochemistry respectively in surgically excised breast tumor tissue. Iodine transport ability and its nature was assessed both in vivo and in vitro. We report high NIS expression at both transcriptional and translational level and its ability to transport iodine in human breast tumors. The in vivo iodine transport ability was confirmed by scintigraphy. Unlike thyroid, perchlorate and thiocyanate do not inhibit iodine transport in breast tumors. The presence of iodinated proteins suggests the longer retention time. The unequivocal demonstration of NIS expression, its functionality and retention of iodine by organification further provides supportive evidence for use of radioiodine as an additional treatment modality of human breast carcinoma.

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Upadhyay, G., Singh, R., Agarwal, G. et al. Functional Expression of Sodium Iodide Symporter (NIS) in Human Breast Cancer Tissue. Breast Cancer Res Treat 77, 157–165 (2003). https://doi.org/10.1023/A:1021321409159

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  • DOI: https://doi.org/10.1023/A:1021321409159

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