Review Article

Metabolic Alterations of Thyroid Cancer as Potential Therapeutic Targets

Table 1

Association between oncogene mutations and metabolic phenotype of thyroid cancer. The table summarizes the association between oncogene activation or tumor suppressor inactivation and alterations of proteins involved in glucose uptake, glycolysis, and glutamine metabolism in thyroid cancer.

Thyroid oncogeneTarget genes/metabolic pathwaysRegulationReference

ā€‰GLUT1, MCT4, HKII, CAIX, PKM2, GLS1, GDH, ASCT2Activated[27, 33, 34]
O2 consumptionInhibited[35]

Ras mutationsATP-synthaseInhibited[36]

PTEN
loss of function
GLUT1Activated[37]

p53 mutationsGLUT1Activated[38, 39]

ASCT2: amino acid transporter-2; CAIX: carbonic anhydrase IX; GLS1: glutaminase; GLUT1: glucose transporter 1; GDH: glutamate dehydrogenase; PKM2: pyruvate kinase isoform M2.