Tumor cell glycolytic metabolism

Tumor cell glycolytic metabolism, commonly known as the "Warburg effect," is defined by the preference of cancer cells for glycolysis over oxidative phosphorylation for ATP production, even in the presence of oxygen[2][5][6]. This metabolic adaptation is driven by oncogenic signaling (such as PI3K/AKT, MYC, and HIF-1α) and loss of tumor suppressors (such as p53), conferring advantages for rapid proliferation, survival in low oxygen environments, and resistance to apoptotic signals[1][4][5]. Glycolytic reprogramming supports increased glucose uptake, upregulation of glycolytic enzymes, and enhanced lactate production. While this metabolic phenotype is a fundamental hallmark of many cancers, it is not itself a molecule, enzyme, or receptor, but a coordinated alteration in cellular metabolism[2][4][5][6]. Many individual components of this pathway (e.g., GLUT1, hexokinase 2, LDHA, PKM2, and HIF-1α) are considered potential direct therapeutic targets in cancer, rather than the entire glycolytic metabolism process[4].

Other names

Tumor glycolysisCancer cell glycolysisWarburg effectAerobic glycolysis in tumors

Inhibition of glucose uptake (e.g., GLUT1 inhibitors); Inhibition of glycolytic enzymes (e.g., hexokinase, pyruvate kinase, LDH inhibitors); Inhibition of HIF-1α or PI3K/AKT pathway, which regulate glycolytic flux