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Growth arrest of thyrotropic tumors by thyroid hormone is correlated with novel changes in Wnt-10A

Janice M Kerr1, David F Gordon, Whitney W Woodmansee

  • 1University of Colorado Health Sciences Center, Department of Medicine, Division of Endocrinology, Metabolism, and Diabetes, MS8106, P.O. Box 6511 Denver, CO 80262, USA. janice.kerr@uchsc.edu

Molecular and Cellular Endocrinology
|May 18, 2005
PubMed

Insights

Thyroid hormone (T3) inhibits thyrotrope cell growth by down-regulating Wnt-10A expression and reducing beta-catenin signaling. This pathway may involve cyclin A regulation, impacting tumor growth.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cancer Research

Background:

  • The precise molecular mechanisms by which thyroid hormone (T3) regulates thyrotrope cell proliferation remain largely unknown.
  • Understanding these mechanisms is crucial for comprehending thyroid hormone's role in pituitary function and potential therapeutic interventions.

Purpose of the Study:

  • To identify novel T3-regulated genes involved in the growth control of thyrotrope tumor cells.
  • To elucidate the molecular pathways through which T3 inhibits thyrotrope cell proliferation.

Main Methods:

  • Utilized Affymetrix MGU74A Genechip microarray analysis to compare gene expression profiles between hypothyroid and T3-treated TtT-97 tumors.
  • Assessed protein and functional levels of beta-catenin and transcript levels of cyclin A.

Main Results:

  • Identified Wnt-10A as a T3-down-regulated gene abundantly expressed in hypothyroid TtT-97 tumors.
  • Observed decreased nuclear beta-catenin protein and function following T3 treatment.
  • Found that TtT-97 tumor growth suppression correlated with reduced cyclin A transcript levels.

Conclusions:

  • Thyroid hormone (T3) treatment leads to decreased Wnt-10A expression in thyrotropic tumors.
  • Thyroid hormone may inhibit thyrotrope cell growth through the regulation of Wnt-10A and subsequent modulation of cyclin A levels.

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