An investigation into sodium-iodide symporter (NIS) dimerization and its impact on radioiodide uptake in thyroid cancer

2017 ◽  
Author(s):  
Rebecca J. Thompson ◽  
Alice Fletcher ◽  
Hannah Nieto ◽  
Mohammed Alshahrani ◽  
Katie Baker ◽  
...  
2014 ◽  
Vol 28 (7) ◽  
pp. 623-631 ◽  
Author(s):  
Nilufer Yildirim-Poyraz ◽  
Aylin Yazgan ◽  
Elif Ozdemir ◽  
Aysegul Gozalan ◽  
Mutlay Keskin ◽  
...  

Autophagy ◽  
2016 ◽  
Vol 12 (7) ◽  
pp. 1195-1205 ◽  
Author(s):  
Theo S. Plantinga ◽  
Marika H. Tesselaar ◽  
Hans Morreau ◽  
Eleonora P. M. Corssmit ◽  
Brigith K. Willemsen ◽  
...  

2019 ◽  
Vol 60 (9) ◽  
pp. 1301-1307 ◽  
Author(s):  
Tadashi Watabe ◽  
Kazuko Kaneda-Nakashima ◽  
Yuwei Liu ◽  
Yoshifumi Shirakami ◽  
Kazuhiro Ooe ◽  
...  

2020 ◽  
Vol 295 (31) ◽  
pp. 10726-10740
Author(s):  
Hongwei Gao ◽  
Peirong Bai ◽  
Lin Xiao ◽  
Mengjia Shen ◽  
Qiuxiao Yu ◽  
...  

Mediator complex subunit 16 (MED16) is a component of the mediator complex and functions as a coactivator in transcriptional events at almost all RNA polymerase II–dependent genes. In this study, we report that the expression of MED16 is markedly decreased in papillary thyroid cancer (PTC) tumors compared with normal thyroid tissues. In vitro, MED16 overexpression in PTC cells significantly inhibited cell migration, enhanced sodium/iodide symporter expression and iodine uptake, and decreased resistance to radioactive 131I (RAI). Conversely, PTC cells in which MED16 had been further knocked down (MED16KD) exhibited enhanced cell migration, epithelial–mesenchymal transition, and RAI resistance, accompanied by decreased sodium/iodide symporter levels. Moreover, cell signaling through transforming growth factor β (TGF-β) was highly activated after the MED16 knockdown. Similar results were obtained in MED12KD PTC cells, and a co-immunoprecipitation experiment verified interactions between MED16 and MED12 and between MED16 and TGF-βR2. Of note, the application of LY2157299, a potent inhibitor of TGF-β signaling, significantly attenuated MED16KD-induced RAI resistance both in vitro and in vivo. In conclusion, our findings indicate that MED16 reduction in PTC contributes to tumor progression and RAI resistance via the activation of the TGF-β pathway.


Surgery ◽  
2020 ◽  
Vol 167 (1) ◽  
pp. 56-63 ◽  
Author(s):  
Timothy M. Ullmann ◽  
Heng Liang ◽  
Maureen D. Moore ◽  
Isra Al-Jamed ◽  
Katherine D. Gray ◽  
...  

2004 ◽  
Vol 183 (3) ◽  
pp. 617-626 ◽  
Author(s):  
Eleonore Fröhlich ◽  
Anja Witke ◽  
Barbara Czarnocka ◽  
Richard Wahl

Retinoids are potential candidates for the treatment of thyroid cancer. However, one of the disadvantages of these substances is their dedifferentiating effect on normal non-transformed thyrocytes. To identify conditions under which no dedifferentiating effect of retinol on normal thyrocytes can be observed, we determined iodide uptake, protein iodination, expression of sodium–iodide symporter (NIS) mRNA and protein, and the binding of iodine-125-labelled bTSH in cultured porcine thyrocytes. Combination of TSH and ≤6.5 μM retinol increased iodide uptake and protein iodination compared with TSH alone over the entire incubation time, whereas TSH plus ≥13 μM retinol increased the uptake of iodine-125 only during the first 12 h but decreased it after 30 h and longer. After ≥30 h incubation times with ≥13 μM retinol, the fraction of apoptotic cells was enhanced and proliferation decreased. The incubation with retinol enhanced the binding of [125I]bTSH to thyrocytes, but did not influence expression of the NIS. With low retinol concentrations, the effect on the binding of TSH apparently predominated and retinol increased thyroid function; with higher concentrations the pro-apoptotic effect of retinol overlapped and a two-phased time course resulted. It can be concluded that low concentrations of retinol also exert differentiating effects in normal thyrocytes.


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