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The Molecular Landscape of Hürthle Cell Thyroid Cancer Is Associated with Altered Mitochondrial Function-A

Sonam Kumari1, Ruth Adewale1, Joanna Klubo-Gwiezdzinska1

  • 1Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Cells
|July 2, 2020
PubMed

Insights

Hürthle cell thyroid carcinoma (HTC) exhibits unique mitochondrial DNA mutations and relies on aerobic glycolysis for energy. Understanding HTC

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Hürthle cell thyroid carcinoma (HTC) represents 3-5% of thyroid cancers, often presenting with aggressive behavior and poor response to radioiodine therapy.
  • The molecular profile of HTC diverges significantly from other thyroid cancer subtypes, suggesting distinct oncogenic pathways.
  • Mitochondrial dysfunction and altered cellular metabolism are increasingly recognized as hallmarks of cancer.

Purpose of the Study:

  • To conduct a comprehensive literature review on the molecular features of HTC and their association with cancer metabolism.
  • To elucidate the specific metabolic dependencies and genetic underpinnings of HTC.
  • To identify potential therapeutic targets based on the unique molecular and metabolic landscape of HTC.

Main Methods:

  • Systematic literature search of PubMed, Embase, and Medline databases (1980-2020).
  • Keywords included "HTC", "genomic analysis", "mutations", "exome sequencing", "molecular", "mitochondria", "metabolism", "oxidative phosphorylation", "glycolysis", "oxidative stress", "reactive oxygen species", and "oncogenes".
  • Review focused on clinical and translational studies linking molecular characteristics to metabolic pathways in HTC.

Main Results:

  • HTC frequently harbors complex I mitochondrial DNA mutations as early genetic events, leading to mitochondrial dysfunction.
  • HTC predominantly utilizes aerobic glycolysis for energy production, with downregulated oxidative phosphorylation-related genes.
  • Enhanced glucose uptake in HTC is exploited for diagnostic imaging, such as fluorodeoxyglucose positron emission tomography (FGD-PET/CT).

Conclusions:

  • The distinct molecular signature of HTC, characterized by mitochondrial DNA mutations and a glycolytic phenotype, differentiates it from other thyroid cancers.
  • Targeting the specific metabolic pathways of HTC may offer novel therapeutic strategies.
  • Further metabolomic profiling integrated with molecular data is crucial for developing personalized treatments for HTC.
Keywords:
Hürthle cellmetabolismmitochondriaoncogenesoxidative phosphorylationthyroid cancer

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