Glucose metabolism pathway in cancer cells

The glucose metabolism pathway in cancer cells, classically known as the Warburg effect, refers to tumor cells' reprogramming of cellular energy production to favor aerobic glycolysis, increasing glucose uptake and lactate production even when oxygen is sufficient[1][2][3][4]. This adaptation supports rapid cancer cell proliferation by supplying ATP and metabolic intermediates needed for biosynthesis[1][3]. Many enzymes and transporters involved in this pathway, such as hexokinase II (HK2), phosphofructokinase (PFK), and pyruvate kinase M2 (PKM2), are upregulated in cancer and have been explored as therapeutic targets[2][4][6]. However, the term is not a single molecular target but a composite description of an altered metabolic network in cancer cells. While drugs targeting various components of this pathway have been developed and investigated (such as 2-deoxyglucose, 3-bromopyruvate, and isoform-selective inhibitors like ivosidenib), clinical application is limited by toxicity and metabolic compensatory mechanisms[2][4][6]. Elevated glucose uptake is also used as a biomarker in cancer diagnostics (e.g., FDG-PET imaging)[1][3].

Other names

Aerobic glycolysis in cancerWarburg effectCancer cell glucose metabolism

- Inhibition of glycolytic enzymes (e.g., HK, PFK, PKM2) - Disruption of glucose uptake - Blockade of lactate production