Smit J W, Schröder-van der Elst J P, Karperien M, Que I, Romijn J A, van der Heide D
Department of Endocrinology and Metabolism, Leiden University Medical Center, The Netherlands.
Exp Clin Endocrinol Diabetes. 2001;109(1):52-5. doi: 10.1055/s-2001-11019.
The uptake of iodide in thyroid epithelial cells is mediated by the sodium/iodide symporter (NIS). The uptake of iodide is of vital importance for thyroid physiology and is a prerequisite for radioiodine therapy in thyroid cancer. Loss of iodide uptake due to diminished expression of the human NIS (hNIS) is frequently observed in metastasized thyroid cancer. So far, no animal model for the study of radioiodine therapy in thyroid cancer has been available. Strategies to restore iodide uptake in thyroid cancer include the exploration of hNIS gene transfer into hNIS defective thyroid cancer. We have performed a stable transfection of hNIS into the hNIS defective follicular thyroid carcinoma cell line FTC133. Stably transfected colonies exhibited high uptake of Na125I, which could be blocked completely with sodium perchlorate. hNIS transfected FTC133 and non-transfected cell lines injected subcutaneously in nude mice formed tumors after 6 weeks. Iodide uptake in the hNIS transfected tumor was much higher than in non-transfected tumor, but a rapid release of radioactivity from the hNIS transfected tumor was observed. Further studies are necessary to investigate the role of hNIS in relation to other thyroid specific proteins in iodide metabolism in thyroid cancer.
甲状腺上皮细胞对碘化物的摄取由钠/碘同向转运体（NIS）介导。碘化物的摄取对甲状腺生理功能至关重要，是甲状腺癌放射性碘治疗的前提条件。在转移性甲状腺癌中，常观察到由于人类NIS（hNIS）表达减少而导致碘化物摄取丧失。到目前为止，尚无用于研究甲状腺癌放射性碘治疗的动物模型。恢复甲状腺癌中碘化物摄取的策略包括探索将hNIS基因转入hNIS缺陷型甲状腺癌。我们已将hNIS稳定转染至hNIS缺陷型滤泡性甲状腺癌细胞系FTC133中。稳定转染的菌落表现出对Na125I的高摄取，这可被高氯酸钠完全阻断。将hNIS转染的FTC133和未转染的细胞系皮下注射到裸鼠中，6周后形成肿瘤。hNIS转染肿瘤中的碘化物摄取远高于未转染肿瘤，但观察到hNIS转染肿瘤中有放射性快速释放。有必要进一步研究hNIS在甲状腺癌碘代谢中与其他甲状腺特异性蛋白相关的作用。
