ArticleJournal of cell science2009
A novel mechanism of sodium iodide symporter repression in differentiated thyroid cancer.
Article in Journal of cell science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 103 citations in OpenAlex.
- Disulfiram metabolite Cu(DDC)EBioMedicine · 2026Article
- Elevated NIS Expression Correlates with Chemoresistance in Triple-Negative Breast Cancer: Potential Link to FOXA1 Activity.Medical sciences (Basel, Switzerland) · 2025Article
- Targeting Src tyrosine kinase to enhance radioiodide uptake in breast cancer.Endocrine-related cancer · 2025Article
- Histological Evaluation of Sodium Iodide-Based Root Canal Filling Materials in Canine Teeth.Materials (Basel, Switzerland) · 2024Article
- Optimization of Sodium Iodide-Based Root Filling Material for Clinical Applications: Enhancing Physicochemical Properties.Pharmaceutics · 2024Article
- Combined Vorinostat and Chloroquine Inhibit Sodium-Iodide Symporter Endocytosis and Enhance Radionuclide Uptake In Vivo.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- The Plasma Membrane Monoamine Transporter is Highly Expressed in Neuroblastoma and Functions as an mIBG Transporter.The Journal of pharmacology and experimental therapeutics · 2023Article
- Advances in the molecular mechanism and targeted therapy of radioactive-iodine refractory differentiated thyroid cancer.Medical oncology (Northwood, London, England) · 2023Review
- Molecular mechanisms of resistance to kinase inhibitors and redifferentiation in thyroid cancers.Endocrine-related cancer · 2022Review
- Basolateral Sorting of the Sodium/Iodide Symporter Is Mediated by Adaptor Protein 1 Clathrin Adaptor Complexes.Thyroid : official journal of the American Thyroid Association · 2022Article
- Redox Homeostasis in Thyroid Cancer: Implications in NaInternational journal of molecular sciences · 2022Review
- Recurrence of Papillary Thyroid Cancer: A Systematic Appraisal of Risk Factors.The Journal of clinical endocrinology and metabolism · 2022Article
- Article
- Targeting non-canonical pathways as a strategy to modulate the sodium iodide symporter.Cell chemical biology · 2022Article
- Mechanisms of regulating NIS transport to the cell membrane and redifferentiation therapy in thyroid cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Review
- Article
- Multimodal Imaging-Based Potential Visualization of the Tumor Microenvironment in Bone Metastasis.Cells · 2021Review
- Na+/I- symporter expression, function, and regulation in non-thyroidal tissues and impact on thyroid cancer therapy.Endocrine-related cancer · 2021Article
- A Novel SLC5A5 Variant Reveals the Crucial Role of Kinesin Light Chain 2 in Thyroid Hormonogenesis.The Journal of clinical endocrinology and metabolism · 2021Article
- Tumor microenvironment affects exogenous sodium/iodide symporter expression.Translational oncology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Differentiated thyroid cancers and their metastases frequently exhibit reduced iodide uptake, impacting on the efficacy of radioiodine ablation therapy. PTTG binding factor (PBF) is a proto-oncogene implicated in the pathogenesis of thyroid cancer. We recently reported that PBF inhibits iodide uptake, and have now elucidated a mechanism by which PBF directly modulates sodium iodide symporter (NIS) activity in vitro. In subcellular localisation studies, PBF overexpression resulted in the redistribution of NIS from the plasma membrane into intracellular vesicles, where it colocalised with the tetraspanin CD63. Cell-surface biotinylation assays confirmed a reduction in plasma membrane NIS expression following PBF transfection compared with vector-only treatment. Coimmunoprecipitation and GST-pull-down experiments demonstrated a direct interaction between NIS and PBF, the functional consequence of which was assessed using iodide-uptake studies in rat thyroid FRTL-5 cells. PBF repressed iodide uptake, whereas three deletion mutants, which did not localise within intracellular vesicles, lost the ability to inhibit NIS activity. In summary, we present an entirely novel mechanism by which the proto-oncogene PBF binds NIS and alters its subcellular localisation, thereby regulating its ability to uptake iodide. Given that PBF is overexpressed in thyroid cancer, these findings have profound implications for thyroid cancer ablation using radioiodine.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.