Figure 1.

Cancer-associated metabolic alterations occurring with the Warburg phenotype. Intrinsic dysregulation of a range of different genes (oncogene activation, as MYC, or loss of tumour suppressor genes, as p53) leads to the activation of downstream pathways, which, ultimately, promote an increase of glucose consumption, glycolytic flux and lactate production. Altogether, the accumulation of extracellular lactate promotes the acidification of the tumour microenvironment, leading to cancer aggressiveness. CD147, cluster of differentiation 147; GLUT1, glucose transporter 1; HIF-1, hypoxia-inducible factor 1; HK2, hexokinase 2; LDHA, lactate dehydrogenase isoform A; MCT1/4, monocarboxylate transporter 1 or 4; p53, tumour protein 53; PFK, phosphofructokinase; PK, pyruvate kinase; TME, tumour microenvironment.