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Updated: May 9, 2025

An Orthotopic Mouse Model of Anaplastic Thyroid Carcinoma
Published on: April 17, 2013
Regulation of iodide transportation by a plant secondary metabolite in SW1736 anaplastic thyroid cancer cell line
Shabnam Heydarzadeh1, Ali Asghar Moshtaghie2, Maryam Daneshpour1
1Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Molecular Biology, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Aims And Background:
Owing to impaired iodine metabolism, anaplastic thyroid carcinoma, recognized as one of the most formidable malignancies, is resistant to radioiodine therapy. This study was conducted to determine the possible role of Genistein as plant secondary metabolite in understanding the effectiveness of this nutraceutical compound in modulating Sodium iodide symporter (NIS) expression and iodide uptake in the SW1736 anaplastic thyroid cancer cell linen.
Material Methods:
Cell viability was assessed using the MTT assay, whereas cell apoptosis was assessed using a flow cytometry assay (Annexin V-FITC Apoptosis Detection kit). To determine iodide uptake by SW1736 cells, a Sandell-Kolthoff reaction-based spectrophotometric assay was performed. QRT-PCR and western blotting were used to measure NIS mRNA and protein levels in SW1736 cells.
Results:
SW1736 cells exhibited time- and dose-dependent growth inhibition in response to Genistein treatment. QRT-PCR analysis revealed that NIS mRNA levels in the Genistein-treated group were significantly (p < 0.05) higher than those in the non-treated group. Accordingly, Western blot analysis revealed that SW1736 cells treated with Genistein expressed a high level of the NIS protein (p < 0.01). Compared with the control group, Genistein increased iodide uptake (p < 0.001) in the thyroid cancer cell line SW1736.
Conclusion:
The expression of NIS and subsequent iodine uptake after Genistein treatment suggest that ATC cells may be becoming more like differentiated thyroid cells, which typically have higher iodine uptake capabilities. However, this redifferentiation does not directly correlate with an increase in sensitivity to radioactive iodine treatment.
Insights
Genistein treatment increases Sodium iodide symporter (NIS) expression and iodide uptake in anaplastic thyroid cancer cells. This suggests potential redifferentiation, though not necessarily increased sensitivity to radioiodine therapy.
Area of Science:
- Oncology
- Molecular Biology
- Nutraceutical Research
Background:
- Anaplastic thyroid carcinoma (ATC) is highly aggressive and resistant to radioiodine therapy due to impaired iodine metabolism.
- Understanding mechanisms to re-sensitize ATC to radioiodine is crucial for improving treatment outcomes.
Purpose of the Study:
- To investigate the effect of Genistein, a plant metabolite, on Sodium iodide symporter (NIS) expression and iodide uptake in SW1736 anaplastic thyroid cancer cells.
- To assess Genistein's role in potentially modulating ATC cell behavior towards a more differentiated state.
Main Methods:
- Cell viability assessed via MTT assay and apoptosis via flow cytometry.
- Iodide uptake measured using a spectrophotometric assay.
- NIS mRNA and protein levels determined by QRT-PCR and Western blotting, respectively.
Main Results:
- Genistein demonstrated time- and dose-dependent inhibition of SW1736 cell growth.
- Genistein significantly upregulated NIS mRNA and protein expression in SW1736 cells (p < 0.05 and p < 0.01, respectively).
- Genistein treatment markedly increased iodide uptake in SW1736 cells (p < 0.001).
Conclusions:
- Genistein treatment appears to induce a redifferentiation-like effect in ATC cells by upregulating NIS expression and enhancing iodide uptake.
- Despite increased iodide uptake, this observed redifferentiation did not translate to increased sensitivity to radioactive iodine treatment.
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