text: Highly malignant tumors rely heavily on anaerobic glycolysis (metabolism of glucose to lactic acid even under ample tissue oxygen; Warburg effect) and thus need to efflux lactic acid via MCTs to the tumor micro-environment to maintain a robust glycolytic flux and to prevent the tumor from being "pickled to death". The MCTs have been successfully targeted in pre-clinical studies using RNAi  and a small-molecule inhibitor alpha-cyano-4-hydroxycinnamic acid (ACCA; CHC) to show that inhibiting lactic acid efflux is a very effective therapeutic strategy against highly glycolytic malignant tumors.
  In some tumor types, growth and metabolism relies on the exchange of lactate between glycolytic and rapidly respiring cells. This is of particular importance during tumor cell development when cells often undergo anaerobic metabolism, as described by the Warburg effect. Other cells in the same tumor may have access to or recruit sources of oxygen (via angiogenesis), allowing it to undergo aerobic oxidation. The lactate shuttle could occur as the hypoxic cells anaerobically metabolize glucose and shuttle the lactate via MCT to the adjacent cells capable of using the lactate as a substrate for oxidation. Investigation into how MCT-mediated lactate exchange in targeted tumor cells can be inhibited, therefore depriving cells of key energy sources, could lead to promising new chemotherapeutics.
  Additionally, lactate has been shown to be a key factor in tumor angiogenesis. Lactate promotes angiogenesis by upregulating HIF-1 in endothelial cells. Thus a promising target of cancer therapy is the inhibition of lactate export, through MCT-1 blockers, depriving developing tumors of an oxygen source.