Expression pattern of the pendrin and sodium/iodide symporter genes in human thyroid carcinoma cell lines and human thyroid tumors

Arturi, Franco; Russo, Diego; Bidart, Jean‐Michel; Scarpelli, Daniela; Schlumberger, Martin; Filetti, Sébastiano

doi:10.1530/eje.0.1450129

Cited by 68 publications

(43 citation statements)

References 30 publications

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“…Further, immunohistochemical assessment, although not formally quantified, showed NIS protein expression to be reduced in papillary and follicular tumour samples compared with normal ( Figure 1c). Thus, in common with several previous reports (Liou et al, 2000;Arturi et al, 2001;Ringel et al, 2001), NIS expression is reduced in our samples of differentiated thyroid cancer compared with normal thyroid tissue.…”

Section: Nis Expression Is Reduced In Thyroid Cancersupporting

confidence: 93%

PTTG and PBF repress the human sodium iodide symporter

et al. 2007

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The ability of the thyroid to accumulate iodide provides the basis for radioiodine ablation of differentiated thyroid cancers and their metastases. Most thyroid tumours exhibit reduced iodide uptake, although the mechanisms accounting for this remain poorly understood. Pituitary tumour transforming gene (PTTG) is a proto-oncogene implicated in the pathogenesis of thyroid tumours. We now show that PTTG and its binding factor PBF repress expression of sodium iodide symporter (NIS) messenger RNA (mRNA), and inhibit iodide uptake. This process is mediated at least in part through fibroblast growth factor-2. In detailed studies of the NIS promoter in rat FRTL-5 cells, PTTG and PBF demonstrated specific inhibition of promoter activity via the human upstream enhancer element (hNUE). Within this B1 kb element, a complex PAX8-upstream stimulating factor 1 (USF1) response element proved critical both to basal promoter activity and to PTTG and PBF repression of NIS. In particular, repression by PTTG was contingent upon the USF1, but not the PAX8, site. Finally, in human primary thyroid cells, PTTG and PBF similarly repressed the NIS promoter via hNUE. Taken together, our data suggest that the reported overexpression of PTTG and PBF in differentiated thyroid cancer has profound implications for activity of the NIS gene, and hence significantly impacts upon the efficacy of radioiodine treatment.

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Section: Nis Expression Is Reduced In Thyroid Cancersupporting

confidence: 93%

PTTG and PBF repress the human sodium iodide symporter

et al. 2007

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“…The first of these is SLC26A4, which encodes for the pendrin (PDS) expressed in apical membranes and has been suggested to transfer iodide into the colloid from the cells. It has previously shown that PDS expression was detected in thyroid (B-CPAP), thyroid cancer (WRO, FRO, ARO) [27] and breast cells (MCF-7) [28]. The other is SLC5A8 (human apical iodide transporter, hAIT), which was suggested to charge the release of iodide into the colloid across the apical membrane as an iodide channel [29,30].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Tanespimycin (17-AAG) on Radioiodine Accumulation in Sodium-Iodide Symporter Expressing Cells

Youn

Song

et al. 2012

Nucl Med Mol Imaging

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Purpose The heat shock protein 90 inhibitor, tanespimycin, is an anticancer agent known to increase iodine accumulation in normal and cancerous thyroid cells. Iodine accumulation is regulated by membrane proteins such as sodium iodide symporter (NIS) and pendrin (PDS), and thus we attempted to characterize the effects of tanespimycin on those genes. Methods Cells were incubated with tanespimycin in order to evaluate 125 I accumulation and efflux ability. Radioiodine uptake and efflux were measured by a gamma counter and normalized by protein amount. RT-PCR were performed to measure the level of gene expression. Results After tanespimycin treatment, 125 I uptake was increased by ∼2.5-fold in FRTL-5, hNIS-ARO, and hNIS-MDA-MB-231 cells, but no changes were detected in the hNIS-HeLa cells. Tanespimycin significantly reduced the radioiodine efflux rate only in the FRTL-5 cells. In the FRTL-5 and hNIS-ARO cells, PDS mRNA levels were markedly reduced; the only other observed alteration in the levels of NIS mRNA after tanespimycin treatment was an observed increase in the hNIS-ARO cells. Conclusions These results indicate that cellular responses against tanespimycin treatment differed between the normal rat thyroid cells and human cancer cells, and the reduction in the 125 I efflux rate by tanespimycin in the normal rat thyroid cells might be attributable to reduced PDS gene expression.

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“…The expression of NIS in thyroid tumours has been investigated by different groups, with variable results. In particular, in a subset of either adenomas or carcinomas, NIS expression appeared to be reduced compared with the corresponding normal tissue (2 -6) or nil (7,8) whereas, in other cases, NIS was equally expressed or overexpressed compared with the normal tissue (9,10). In the latter case, NIS protein showed a defective targeting to the cell membrane and was mostly located inside the cytoplasm.…”

Section: Introductionmentioning

confidence: 93%

Expression of cAMP response element-binding protein and sodium iodide symporter in benign non-functioning and malignant thyroid tumours

Luciani

Buci²,

Conforti³

et al. 2003

European Journal of Endocrinology

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Objective: Reduced expression or defective targeting of the sodium/iodide symporter (NIS) to the cell membrane in thyroid tumours has been reported. The expression of the NIS gene is up-regulated by TSH through the cAMP pathway and the characterization of the promoter region of the rat NIS gene revealed the existence of a degenerate cAMP response element (CRE) sequence. The cAMPdependent transcription factor cAMP response element-binding protein (CREB) binds to CRE acting, upon phosphorylation, as a transcriptional activator. In this study we evaluated the expression of CREB and NIS gene in thyroid non-functioning adenomas ðn ¼ 18Þ and carcinomas ðn ¼ 20Þ; as well as in the corresponding normal tissue. Methods: The levels of CREB and NIS mRNA were determined by quantitative real-time RT-PCR, whereas CREB protein (total and phosphorylated) was analyzed by Western blot. Results: The levels of CREB mRNA in thyroid carcinomas, but not in adenomas, were significantly lower than in the corresponding normal tissue ð4:63^0:89 vs 9:51^2:01 pg/mg total RNA, meansŜ .E., P ¼ 0:025Þ: CREB protein levels, which were determined in a subset of samples, were in quite good agreement with mRNA data. NIS mRNA levels did not differ in adenomas or carcinomas, compared with the corresponding normal tissue and no significant relationship with the levels of CREB mRNA was observed. Conclusions: Our results have indicated for the first time that reduced levels of CREB expression are a feature of thyroid carcinomas, and confirm that different factors are likely to modulate NIS expression.

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Expression pattern of the pendrin and sodium/iodide symporter genes in human thyroid carcinoma cell lines and human thyroid tumors

Cited by 68 publications

References 30 publications

PTTG and PBF repress the human sodium iodide symporter

PTTG and PBF repress the human sodium iodide symporter

The Effect of Tanespimycin (17-AAG) on Radioiodine Accumulation in Sodium-Iodide Symporter Expressing Cells

Expression of cAMP response element-binding protein and sodium iodide symporter in benign non-functioning and malignant thyroid tumours

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