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Mitochondrial Metabolism as a Treatment Target in Anaplastic Thyroid Cancer

Jennifer M Johnson1, Stephen Y Lai2, Paolo Cotzia3

  • 1Department of Medical Oncology, Thomas Jefferson University, Philadelphia, PA.

Seminars in Oncology
|November 29, 2015
PubMed

Insights

Anaplastic thyroid cancer (ATC) exhibits distinct mitochondrial features, with high expression of monocarboxylate transporter 1 (MCT1) and translocase of the outer mitochondrial membrane member 20 (TOMM20). Targeting MCT1 may offer a novel therapeutic strategy for ATC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Research

Background:

  • Anaplastic thyroid cancer (ATC) is a highly aggressive malignancy.
  • Mitochondrial metabolism is often dysregulated in ATC.
  • Identifying specific metabolic vulnerabilities is crucial for targeted therapies.

Purpose of the Study:

  • To define the mitochondrial metabolic phenotype of ATC.
  • To investigate the expression of monocarboxylate transporter 1 (MCT1) and translocase of the outer mitochondrial membrane member 20 (TOMM20) in ATC.
  • To compare metabolic markers between ATC, papillary thyroid cancer (PTC), and non-cancerous thyroid tissue.

Main Methods:

  • Analysis of MCT1 and TOMM20 expression in human thyroid tissue samples (ATC, PTC, non-cancerous) and ATC mouse xenografts.
  • Utilized visual and digital scoring for staining patterns.
  • Assessed (13)C-pyruvate uptake in xenograft tumors.

Main Results:

  • MCT1 demonstrated significantly higher expression in ATC compared to PTC and non-cancerous thyroid tissue.
  • TOMM20 was highly expressed in both ATC and PTC relative to non-cancerous thyroid tissue.
  • ATC mouse xenografts showed elevated MCT1 and TOMM20 expression and high (13)C-pyruvate uptake.

Conclusions:

  • ATC possesses unique metabolic characteristics, notably high MCT1 and TOMM20 expression, differentiating it from PTC and normal thyroid tissue.
  • PTC shows low MCT1 expression, while non-cancerous tissue has low expression of both markers.
  • MCT1 blockade presents a potential targeted therapeutic strategy specifically for anaplastic thyroid cancer.

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