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Molecular Cancer Research
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Cancer Genes and Networks

Thyroid Hormone Receptor Beta Induces a Tumor-Suppressive Program in Anaplastic Thyroid Cancer

Eric L. Bolf, Noelle E. Gillis, Cole D. Davidson, Princess D. Rodriguez, Lauren Cozzens, Jennifer A. Tomczak, Seth Frietze and Frances E. Carr
Eric L. Bolf
1Department of Pharmacology, Larner College of Medicine, Burlington, Vermont.
2University of Vermont Cancer Center, Burlington, Vermont.
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Noelle E. Gillis
1Department of Pharmacology, Larner College of Medicine, Burlington, Vermont.
2University of Vermont Cancer Center, Burlington, Vermont.
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  • ORCID record for Noelle E. Gillis
Cole D. Davidson
1Department of Pharmacology, Larner College of Medicine, Burlington, Vermont.
2University of Vermont Cancer Center, Burlington, Vermont.
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Princess D. Rodriguez
3Department of Biomedical and Health Sciences, College of Nursing and Health Sciences, University of Vermont, Burlington, Vermont.
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Lauren Cozzens
1Department of Pharmacology, Larner College of Medicine, Burlington, Vermont.
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Jennifer A. Tomczak
1Department of Pharmacology, Larner College of Medicine, Burlington, Vermont.
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Seth Frietze
2University of Vermont Cancer Center, Burlington, Vermont.
3Department of Biomedical and Health Sciences, College of Nursing and Health Sciences, University of Vermont, Burlington, Vermont.
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Frances E. Carr
1Department of Pharmacology, Larner College of Medicine, Burlington, Vermont.
2University of Vermont Cancer Center, Burlington, Vermont.
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  • For correspondence: fcarr@uvm.edu
DOI: 10.1158/1541-7786.MCR-20-0282 Published October 2020
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Abstract

The thyroid hormone receptor beta (TRβ), a key regulator of cellular growth and differentiation, is frequently dysregulated in cancers. Diminished expression of TRβ is noted in thyroid, breast, and other solid tumors and is correlated with more aggressive disease. Restoration of TRβ levels decreased tumor growth supporting the concept that TRβ could function as a tumor suppressor. Yet, the TRβ tumor suppression transcriptome is not well delineated and the impact of TRβ is unknown in aggressive anaplastic thyroid cancer (ATC). Here, we establish that restoration of TRβ expression in the human ATC cell line SW1736 (SW-TRβ) reduces the aggressive phenotype, decreases cancer stem cell populations and induces cell death in a T3-dependent manner. Transcriptomic analysis of SW-TRβ cells via RNA sequencing revealed distinctive expression patterns induced by ligand-bound TRβ and revealed novel molecular signaling pathways. Of note, liganded TRβ repressed multiple nodes in the PI3K/AKT pathway, induced expression of thyroid differentiation markers, and promoted proapoptotic pathways. Our results further revealed the JAK1–STAT1 pathway as a novel, T3-mediated, antitumorigenic pathway that can be activated in additional ATC lines. These findings elucidate a TRβ-driven tumor suppression transcriptomic signature, highlight unexplored therapeutic options for ATC, and support TRβ activation as a promising therapeutic option in cancers.

Implications: TRβ-T3 induced a less aggressive phenotype and tumor suppression program in anaplastic thyroid cancer cells revealing new potential therapeutic targets.

Footnotes

  • Note: Supplementary data for this article are available at Molecular Cancer Research Online (http://mcr.aacrjournals.org/).

  • Mol Cancer Res 2020;18:1443–52

  • Received March 26, 2020.
  • Revision received April 24, 2020.
  • Accepted June 11, 2020.
  • Published first June 17, 2020.
  • ©2020 American Association for Cancer Research.
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Molecular Cancer Research: 18 (10)
October 2020
Volume 18, Issue 10
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Thyroid Hormone Receptor Beta Induces a Tumor-Suppressive Program in Anaplastic Thyroid Cancer
Eric L. Bolf, Noelle E. Gillis, Cole D. Davidson, Princess D. Rodriguez, Lauren Cozzens, Jennifer A. Tomczak, Seth Frietze and Frances E. Carr
Mol Cancer Res October 1 2020 (18) (10) 1443-1452; DOI: 10.1158/1541-7786.MCR-20-0282

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Thyroid Hormone Receptor Beta Induces a Tumor-Suppressive Program in Anaplastic Thyroid Cancer
Eric L. Bolf, Noelle E. Gillis, Cole D. Davidson, Princess D. Rodriguez, Lauren Cozzens, Jennifer A. Tomczak, Seth Frietze and Frances E. Carr
Mol Cancer Res October 1 2020 (18) (10) 1443-1452; DOI: 10.1158/1541-7786.MCR-20-0282
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Molecular Cancer Research
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