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Davidson et al. J Cancer Metastasis Treat 2021;7:45 Journal of Cancer
DOI: 10.20517/2394-4722.2021.77
Metastasis and Treatment

Review Open Access

Review of pharmacological inhibition of thyroid
cancer metabolism

1,2
Cole D. Davidson , Frances E. Carr 1,2
1
Department of Pharmacology, Larner College of Medicine, Burlington, VT 05405, USA.
2
University of Vermont Cancer Center, Burlington, VT 05405, USA.
Correspondence to: Dr. Frances Carr, Department of Pharmacology, University of Vermont, 149 Beaumont Ave, Burlington, VT
05405, USA. E-mail: Frances.Carr@uvm.edu
How to cite this article: Davidson CD, Carr FE. Review of pharmacological inhibition of thyroid cancer metabolism. J Cancer
Metastasis Treat 2021;7:45. https://dx.doi.org/10.20517/2394-4722.2021.77
Received: 27 Mar 2021 First Decision: 10 May 2021 Revised: 17 May 2021 Accepted: 9 Jun 2021 First online: 15 Jun 2021

Academic Editors: Jerome M. Hershman, Lucio Miele Copy Editor: Yue-Yue Zhang Production Editor: Yue-Yue Zhang

Abstract
Thyroid cancer (TC) is the most common malignancy of the endocrine system and has been rapidly increasing in
incidence over the past few decades. Aggressive TCs metastasize quickly and often levy poor prognoses, as they
are frequently resistant to first-line treatment options. Patients diagnosed with aggressive, dedifferentiated TC
have a prognosis of under a year with the most current treatment modalities. Like many cancers, TCs also exhibit
altered cell metabolism, which enhances the cell’s ability to generate energy, protect against reactive oxygen
species, and synthesize macromolecules such as lipids, proteins, and nucleotides for proliferation. Genetic and
enzyme profiling of TC tissues and cell lines have uncovered several dysregulated metabolic pathways such as
glycolysis, the pentose phosphate pathway, glutamine metabolism, and pyrimidine synthesis. These aberrations are
most often due to overexpression of rate-limiting enzymes or metabolite transporters. Metabolic pathways pose
attractive therapeutic targets in aggressive TC and may serve to work in tandem with standard therapeutics such
as kinase inhibitors depending on the genetic, metabolic, and signaling backgrounds of individual tumors. Further
studies are needed to clearly delineate altered metabolic targets across TC subtypes for implementing therapeutic
metabolic inhibitors that have shown success in other aggressive tumors.

Keywords: Thyroid cancer, tumor metabolism, metabolic inhibitors, Warburg effect, cell signaling

© The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0
International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing,
adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as
long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and
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