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Novel non-genomic signaling of thyroid hormone receptors in thyroid carcinogenesis

Celine J Guigon1, Sheue-yann Cheng

  • 1Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-4264, USA.

Molecular and Cellular Endocrinology
|June 25, 2009
PubMed

Insights

A mutated thyroid hormone receptor (TRbetaPV) acts as an oncogene, driving thyroid cancer through non-genomic actions. This mutant receptor interacts with proteins involved in cell growth and metastasis.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Thyroid hormone receptors (TRs) are transcription factors regulating thyroid hormone (T3) activity.
  • Mutations in TRs are linked to human cancers, with a specific mutation in mice causing thyroid carcinoma.
  • The TRbetaPV mutant mouse model exhibits spontaneous follicular thyroid carcinoma.

Purpose of the Study:

  • To investigate the mechanisms by which the TRbetaPV mutant contributes to thyroid carcinogenesis.
  • To explore the novel non-genomic actions of the TRbetaPV mutant in cancer development.

Main Methods:

  • Utilizing the TRbetaPV/PV mouse model with a germ-line mutation in the Thrbeta gene.
  • Analyzing the physical interactions of the TRbetaPV mutant with key cellular proteins.
  • Investigating the role of these interactions in cell proliferation, motility, migration, and metastasis.

Main Results:

  • The TRbetaPV mutant lacks T3-binding activity and exhibits dominant-negative effects.
  • TRbetaPV directly interacts with phosphatidylinositol 3-kinase regulatory subunit (p85alpha), pituitary tumor transforming gene (PTTG), and beta-catenin.
  • These interactions are crucial for processes driving thyroid cancer progression.

Conclusions:

  • The TRbetaPV mutant functions as an oncogene in thyroid carcinogenesis.
  • Novel non-genomic actions of TRbetaPV, involving protein-protein interactions, are critical for its oncogenic activity.
  • This study reveals a new pathway in thyroid cancer development mediated by mutant TRbeta.

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