{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,27]],"date-time":"2025-11-27T08:41:37Z","timestamp":1764232897603,"version":"3.46.0"},"reference-count":38,"publisher":"The Endocrine Society","issue":"12","license":[{"start":{"date-parts":[[2025,10,23]],"date-time":"2025-10-23T00:00:00Z","timestamp":1761177600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Northern New England Clinical and Translational Research Network (","award":["U54 GM115516"],"award-info":[{"award-number":["U54 GM115516"]}]},{"name":"University of Vermont Cancer Center"},{"DOI":"10.13039\/100018583","name":"Larner College of Medicine, University of Vermont","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100018583","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,11,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Anaplastic thyroid cancer (ATC) is one of the most lethal endocrine cancers with no enduring therapies. Thyroid hormone receptor \u03b2 (TR\u03b2), a recognized tumor suppressor, modulates the transcriptome altering gene expression in numerous intracellular signaling pathways. Our recent studies revealed that TR\u03b2 agonism inhibits glycogen metabolism in ATC cells. Our goal in the present study was to delineate the molecular mechanisms by which TR\u03b2 regulates glycogen synthesis and breakdown. In ATC cells, activation of TR\u03b2 induced changes in expression of genes and proteins in glycogen signaling concordant with downregulation of cancer metabolism. The impact on the cancer cell metabolic phenotype was determined by glycogen levels, cell viability, and reactive oxygen species characterization. Our results revealed that TR\u03b2 activation differentially regulates glycogen signaling pathways reflective of the genetic landscape of the cells. This suggests TR\u03b2 can suppress tumor growth and progression through multiple steps in glycogen metabolism, giving it a unique and distinct role in fine-tuning the microenvironment of the cell as an internal sensor of the general environment of the cell. These studies reveal the potential of a synergistic effect of TR\u03b2 agonism and inhibition of glycogen metabolism in the treatment of aggressive dedifferentiated thyroid cancers.<\/jats:p>","DOI":"10.1210\/endocr\/bqaf156","type":"journal-article","created":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T11:45:38Z","timestamp":1761133538000},"source":"Crossref","is-referenced-by-count":0,"title":["Thyroid Hormone Receptor \u03b2 Suppresses Cancer Cell Activity by Differential Regulation of Glycogen Metabolism"],"prefix":"10.1210","volume":"166","author":[{"ORCID":"https:\/\/orcid.org\/0009-0000-5380-7463","authenticated-orcid":false,"given":"Justin M","family":"Zielinski","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Larner College of Medicine, University of Vermont , Burlington, VT 05405 ,","place":["USA"]},{"name":"Department of Pharmacology, Larner College of Medicine, University of Vermont , Burlington, VT 05405 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