Glucose metabolism pathway in hepatocellular carcinoma cells

Glucose metabolism in hepatocellular carcinoma (HCC) cells refers to the reprogrammed metabolic state where tumor cells prioritize glycolysis over oxidative phosphorylation, a phenomenon known as the Warburg effect (Sun et al., 2018, PubMed: 29951511). This pathway involves the rapid uptake of glucose via transporters like Glucose transporter 1 (GLUT1) and its subsequent conversion to lactate by enzymes such as Hexokinase 2 (HK2) and Lactate dehydrogenase A (LDHA) (DeBerardinis et al., 2008, PubMed: 18177721). These metabolic adaptations provide the necessary energy and carbon skeletons required for the rapid biosynthesis and proliferation of cancer cells. In HCC, this pathway is often regulated by oncogenic signaling through the PI3K/Akt/mTOR and HIF-1α axes (Bader et al., 2005, PubMed: 16151430). While the pathway itself is a critical driver of disease progression, it represents a broad biological process rather than a single, discrete molecular target. Therapeutic interventions targeting this pathway typically involve small molecules designed to inhibit specific rate-limiting enzymes or transporters (Zhang et al., 2014, PubMed: 24561527). However, targeting central metabolism poses significant challenges due to the potential for systemic toxicity in normal, glucose-dependent tissues. Consequently, this entry is classified as a biological pathway context rather than a specific therapeutic target molecule.

Other names

Warburg effect in HCCGlycolytic pathway in liver cancerHCC metabolic reprogrammingAltered glucose metabolism in hepatocellular carcinoma

Inhibition of glycolytic enzymes and glucose transporters to disrupt ATP production and biosynthetic pathways.