Table 1.
Protein | Role in the energetic metabolism | Alterations reported in cancer contexts | References |
---|---|---|---|
GLUT1 | Glucose transport through plasma membrane |
Activation of isoforms 1 and 3 in mammalian tumor models. Its silencing, concomitant with LDH, reduces the tumor phenotype observed upon Notch activation in Drosophila imaginal discs |
34,38 |
Pyruvate Kinase (PK) | Conversion of Phosphoenolpyruvate into pyruvate | Increase of a PKM2 isoform in several mammalian tumor models | 39,40 |
Mitochondrial Pyruvate Carrier (MPC) | Mitochondrial transporters of pyruvate |
Inhibition of isoforms 1 and 2 in mammalian tumor models. Its silencing in Drosophila leads to larval lethality when development occurs in media lacking a carbon source other than sucrose |
41,42 |
Monocarboxylate Transporter (MCT)/Silnoon and Chaski | Transporters of lactate and pyruvate in the plasma membrane | Heightened expression of isoform 4 in mammalian tumor models | 43 |
Pyruvate Dehydrogenase Kinase (PDHK) | Inhibition of the Pyruvate Dehydrogenase complex | Increase in Isoform 1 in several mammalian tumor models | 44,45 |
Lactate Dehydrogenase (LDH)/Impl3 | Reduction of pyruvate and lactate synthesis |
Increase in LDHA isoform in several mammalian tumor models Transformation from hyperplasia to neoplasia depends on LDH activity |
37,46 |
The table summarizes the physiological role of each of the genes in metabolism as well as the nature of the alteration in tumorigenesis.