scholarly journals A Thyroid-Specific Far-Upstream Enhancer in the Human Sodium/Iodide Symporter Gene Requires Pax-8 Binding and Cyclic Adenosine 3′,5′-Monophosphate Response Element-Like Sequence Binding Proteins for Full Activity and Is Differentially Regulated in Normal and Thyroid Cancer Cells

2002 ◽  
Vol 16 (10) ◽  
pp. 2266-2282 ◽  
Author(s):  
Katsumi Taki ◽  
Takahiko Kogai ◽  
Yoko Kanamoto ◽  
Jerome M. Hershman ◽  
Gregory A. Brent
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Sodium Iodide ◽  
Binding Proteins ◽  
Sodium Iodide Symporter ◽  
Response Element ◽  
Full Activity ◽  
Thyroid Cancer Cells

Cyclic AMP–Response Element Modulator Inhibits the Promoter Activity of the Sodium Iodide Symporter Gene in Thyroid Cancer Cells

Thyroid ◽  
2012 ◽  
Vol 22 (5) ◽  
pp. 487-493 ◽  
Author(s):  
Nadia Passon ◽  
Cinzia Puppin ◽  
Elisa Lavarone ◽  
Elisa Bregant ◽  
Alessandra Franzoni ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cyclic Amp ◽  
Cancer Cells ◽  
Promoter Activity ◽  
Sodium Iodide ◽  
Sodium Iodide Symporter ◽  
Response Element ◽  
Cyclic Amp Response Element ◽  
Thyroid Cancer Cells

Dual inhibition of BRAF and MEK increases expression of sodium iodide symporter in patient-derived papillary thyroid cancer cells in vitro

Surgery ◽  
2020 ◽  
Vol 167 (1) ◽  
pp. 56-63 ◽  
Author(s):  
Timothy M. Ullmann ◽  
Heng Liang ◽  
Maureen D. Moore ◽  
Isra Al-Jamed ◽  
Katherine D. Gray ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Sodium Iodide ◽  
Papillary Thyroid ◽  
Sodium Iodide Symporter ◽  
Dual Inhibition ◽  
Thyroid Cancer Cells

scholarly journals Selumetinib Activity in Thyroid Cancer Cells: Modulation of Sodium Iodide Symporter and Associated miRNAs

2018 ◽  
Vol 19 (7) ◽  
pp. 2077 ◽  
Author(s):  
Sabine Wächter ◽  
Annette Wunderlich ◽  
Brandon Greene ◽  
Silvia Roth ◽  
Moritz Elxnat ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Sodium Iodide ◽  
Thyroid Cancer Cell ◽  
Sodium Iodide Symporter ◽  
Radioiodine Uptake ◽  
Thyroid Cancer Cell Lines ◽  
Thyroid Cancer Cells

Background: The MEK (mitogen-activated protein kinase)–inhibitor selumetinib led to increased radioiodine uptake and retention in a subgroup of patients suffering from radioiodine refractory differentiated thyroid cancer (RR-DTC). We aimed to analyse the effect of selumetinib on the expression of sodium iodide symporter (NIS; SLC5A5) and associated miRNAs in thyroid cancer cells. Methods: Cytotoxicity was assessed by viability assay in TPC1, BCPAP, C643 and 8505C thyroid cancer cell lines. NIS, hsa-let-7f-5p, hsa-miR-146b-5p, and hsa-miR-146b-3p expression was determined by quantitative RT-PCR. NIS protein was detected by Western blot. Radioiodine uptake was performed with a Gamma counter. Results: Selumetinib caused a significant reduction of cell viability in all thyroid cancer cell lines. NIS transcript was restored by selumetinib in all cell lines. Its protein level was found up-regulated in TPC1 and BCPAP cells and down-regulated in C643 and 8505C cells after treatment with selumetinib. Treatment with selumetinib caused a down-regulation of hsa-let-7f-5p, hsa-miR-146b-5p and hsa-miR-146b-3p in TPC1 and BCPAP cells. In 8505C cells, a stable or down-regulated hsa-miR-146b-5p was detected after 1h and 48h of treatment. C643 cells showed stable or up-regulated hsa-let-7f-5p, hsa-miR-146b-5p and hsa-miR-146b-3p. Selumetinib treatment caused an increase of radioiodine uptake, which was significant in TPC1 cells. Conclusions: The study shows for the first time that selumetinib restores NIS by the inhibition of its related targeting miRNAs. Further studies are needed to clarify the exact mechanism activated by hsa-miR-146b-5p, hsa-miR-146b-3p and hsa-let7f-5p to stabilise NIS. Restoration of NIS could represent a milestone for the treatment of advanced RR-DTC.

scholarly journals Induction of Thyroid Gene Expression and Radioiodine Uptake in Thyroid Cancer Cells by Targeting Major Signaling Pathways

2010 ◽  
Vol 95 (2) ◽  
pp. 820-828 ◽  
Author(s):  
Peng Hou ◽  
Ermal Bojdani ◽  
Mingzhao Xing
Keyword(s):  
Gene Expression ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Histone Deacetylase ◽  
Sodium Iodide ◽  
Therapeutic Potential ◽  
Sodium Iodide Symporter ◽  
Thyroid Cells ◽  
Thyroid Cancer Cells

Abstract Context: Radioiodine ablation is commonly used to treat thyroid cancer, but a major challenge is often the loss of radioiodine avidity of the cancer caused by aberrant silencing of iodide-handling genes. Objectives: This study was conducted to test the therapeutic potential of targeting the aberrantly activated MAPK and PI3K/Akt/mTOR pathways and histone deacetylase to restore radioiodine avidity in thyroid cancer cells. Experimental Design: We tested the effects of specific inhibitors targeting these pathways/molecules that had established clinical applicability, including the MAPK kinase inhibitor RDEA119, mTOR inhibitor temsirolimus, Akt inhibitor perifosine, and histone deacetylase inhibitor SAHA, individually or in combinations, on the expression of iodide-handling genes and radioiodide uptake in a large panel of thyroid cancer cell lines. Results: The expression of a large number of iodide-handling genes could be restored, particularly the sodium/iodide symporter, TSH receptor, and thyroperoxidase, by treating cells with these inhibitors. The effect was particularly robust and synergistic when combinations of inhibitors containing SAHA were used. Robust expression of sodium/iodide symporter in the cell membrane, which plays the most important role in iodide uptake in thyroid cells, was confirmed by immunofluorescent microscopy. Radioiodide uptake by cells was correspondingly induced under these conditions. Thyroid gene expression and radioiodide uptake could both be further enhanced by TSH. Conclusions: Targeting major signaling pathways could restore thyroid gene expression and radioiodide uptake in thyroid cancer cells. Further studies are warranted to test this therapeutic potential in restoring radioiodine avidity of thyroid cancer cells for effective ablation treatment.

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