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<p>Thyroid cancer (TC) is a common endocrine malignancy with rapidly increasing global incidence. Clinical management remains challenging for advanced and radioiodine-refractory thyroid cancer (RAIR-TC). Metabolic reprogramming, especially enhanced aerobic glycolysis (the Warburg effect), is a core hallmark of TC that drives tumor progression and therapeutic resistance. This review systematically summarizes the molecular mechanisms of glucose metabolic reprogramming in TC, focusing on key oncogenic drivers including BRAF V600E mutation, RAS mutation, and RET/PTC rearrangement, as well as their downstream mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathways. These pathways coordinately upregulate critical glycolytic regulators: glucose transporter 1 (GLUT1), hexokinase 2 (HK2), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA). We further discuss emerging therapeutic strategies targeting glucose metabolism and highlight challenges including isoform-specific regulation and biomarker-driven patient stratification. This review provides a conceptual framework for translating metabolic insights into improved diagnosis and therapy for TC.</p>

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Glucose Metabolic Reprogramming in Thyroid Cancer: Underlying Molecular Mechanisms and Links to Progression and Treatment

  • 期刊论文

  • 发表日期：

    2026年5月13日

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  • Yi-meng Zhang,
  • Xin-yu Zeng,
  • Yuan Wang,
  • Chen Yang,
  • Jian-qi Bai,
  • Jian-peng Wang,
  • Shan He,
  • Ping Zhang

摘要

Thyroid cancer (TC) is a common endocrine malignancy with rapidly increasing global incidence. Clinical management remains challenging for advanced and radioiodine-refractory thyroid cancer (RAIR-TC). Metabolic reprogramming, especially enhanced aerobic glycolysis (the Warburg effect), is a core hallmark of TC that drives tumor progression and therapeutic resistance. This review systematically summarizes the molecular mechanisms of glucose metabolic reprogramming in TC, focusing on key oncogenic drivers including BRAF V600E mutation, RAS mutation, and RET/PTC rearrangement, as well as their downstream mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathways. These pathways coordinately upregulate critical glycolytic regulators: glucose transporter 1 (GLUT1), hexokinase 2 (HK2), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA). We further discuss emerging therapeutic strategies targeting glucose metabolism and highlight challenges including isoform-specific regulation and biomarker-driven patient stratification. This review provides a conceptual framework for translating metabolic insights into improved diagnosis and therapy for TC.