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Type 2 deiodinase is expressed in anaplastic thyroid carcinoma and its inhibition causes cell senescence

Maria Angela De Stefano1, Tommaso Porcelli1, Raffaele Ambrosio2

  • 1Department of Public Health, University of Naples 'Federico II', Naples, Italy.

Endocrine-Related Cancer
|March 6, 2023
PubMed

Insights

Type 2 deiodinase (D2) is highly expressed in anaplastic thyroid cancer (ATC), driving cancer cell proliferation and invasiveness. Inhibiting D2 halts ATC growth and reduces its invasive potential, offering a potential new therapeutic target.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Anaplastic thyroid cancer (ATC) often arises from dedifferentiated papillary or follicular thyroid cancer.
  • Type 2 deiodinase (D2) activates thyroid hormone, is downregulated in papillary thyroid cancer, and linked to skin cancer progression.
  • The role of D2 in ATC pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the expression and function of D2 in anaplastic thyroid cancer.
  • To determine if D2 activity is required for ATC cell proliferation and invasiveness.
  • To explore the relationship between mutated p53 and D2 expression in thyroid cancer.

Main Methods:

  • Comparison of D2 expression in anaplastic versus papillary thyroid cancer cell lines.
  • Assessment of D2 inhibition effects on ATC cell proliferation, cell cycle, senescence, migration, and invasion.
  • Transfection studies to evaluate the impact of mutated p53 on D2 expression.

Main Results:

  • D2 is significantly upregulated in anaplastic thyroid cancer cell lines compared to papillary thyroid cancer.
  • D2-derived tri-iodothyronine (T3) is essential for ATC cell proliferation.
  • D2 inhibition leads to cell cycle arrest (G1), senescence induction, and decreased migration and invasion.
  • Mutated p53 (p5372R(R248W)) can induce D2 expression in papillary thyroid cancer cells.

Conclusions:

  • D2 plays a critical role in the proliferation and invasiveness of anaplastic thyroid cancer.
  • Targeting D2 represents a promising therapeutic strategy for ATC treatment.
  • Mutated p53 may contribute to ATC development by upregulating D2 expression.
Keywords:
anaplastic thyroid cancercell senescencedeiodinasesp53thyroid cancerthyroid hormone

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