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A novel mechanism of sodium iodide symporter repression in differentiated thyroid cancer

Vicki E Smith1, Martin L Read, Andrew S Turnell

  • 1School of Clinical and Experimental Medicine, Institute of Biomedical Research, University of Birmingham B15 2TH, UK.

Journal of Cell Science
|August 27, 2009
PubMed

Insights

The proto-oncogene PTTG binding factor (PBF) directly interacts with the sodium iodide symporter (NIS) in thyroid cancer cells. This interaction causes reduced iodide uptake, potentially impacting radioiodine therapy efficacy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Differentiated thyroid cancers often show reduced iodide uptake, limiting radioiodine ablation therapy effectiveness.
  • PTTG binding factor (PBF), a proto-oncogene, is involved in thyroid cancer development and previously shown to inhibit iodide uptake.

Purpose of the Study:

  • To elucidate the mechanism by which PBF modulates sodium iodide symporter (NIS) activity and iodide uptake in vitro.
  • To investigate the direct interaction between PBF and NIS and its functional consequences.

Main Methods:

  • Subcellular localization studies using PBF overexpression.
  • Cell-surface biotinylation assays to assess plasma membrane NIS expression.
  • Coimmunoprecipitation and GST-pull-down assays to confirm NIS-PBF interaction.
  • In vitro iodide uptake studies in rat thyroid FRTL-5 cells.

Main Results:

  • PBF overexpression caused NIS to redistribute from the plasma membrane to intracellular vesicles, colocalizing with CD63.
  • Cell-surface biotinylation confirmed decreased plasma membrane NIS expression upon PBF transfection.
  • Direct binding between NIS and PBF was demonstrated.
  • PBF significantly repressed iodide uptake; deletion mutants lacking intracellular localization lost inhibitory function.

Conclusions:

  • A novel mechanism identified where PBF directly binds NIS, altering its subcellular localization and inhibiting iodide uptake.
  • PBF's role in regulating NIS activity has significant implications for understanding and potentially improving radioiodine ablation therapy in thyroid cancer, where PBF is overexpressed.

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