Table 1.

Stage-dependent alterations in cancer cell metabolism.

	Cause	Effect	Potential treatment
Intrinsic (Warburg)	P53-deficient tumor cells do not have functional SCO2 or TIGAR and display a glycolytic metabolism phenotype	Protect from apoptosis by closing Kv channels and preventing the influx of calcium	Dichloroacetate, lonidamine
	Embryonic M2 isoform of pyruvate kinase shifts cellular metabolism to aerobic glycolysis	Satisfaction of anabolic requirements, biosynthetic activities by proliferating tumor cells entail the production of ribose-5-phosphate for nucleotide biosynthesis, and the production of fatty acids for lipid biosynthesis
Deadhesion	Deadherent cells suffer deficit in glucose transport, resulting in adenosine triphosphate (ATP) deficiency and anoikis	Peroxide signaling, increased mitochondrial activity	Anti-oxidants
		Serine–glycine–creatine pathway regenerates ATP
Stromal interaction	Lactate secretion from mesenchymal cells via the transporter MCT4	Tumor cells import this lactate via MCT1 expression, converting it to pyruvate and introducing it into the Krebs cycle, resulting increased in oxidative phosphorylation and ATP production
Hypoxia	Hypoxia, low-glucose, lactate	Induction of HIF-1, carbonic anhydrase IX	Methazolamide