cancermetabolism

cancermetabolism refers to the alterations in cellular metabolism that support the growth, survival, and spread of cancer cells. It encompasses changes in energy production, biosynthesis, and redox balance that distinguish malignant cells from their normal counterparts. A central feature is the Warburg effect, in which cancer cells favor high-rate glycolysis and lactate production even when oxygen is plentiful, providing carbon for nucleotide, lipid, and protein synthesis. Mitochondrial oxidative phosphorylation often remains active as well, contributing ATP generation and metabolic intermediates for biosynthesis.

In addition to glycolysis, cancer cells rely on other fuel sources. Glutamine metabolism becomes a major supplier of carbon and nitrogen for nucleotide and amino acid production and helps sustain redox homeostasis through glutathione synthesis. Altered lipid metabolism, including increased fatty acid synthesis and uptake, supports membrane biogenesis and signaling. The tumor microenvironment, hypoxia, and metabolic coupling with stromal and immune cells further shape flux through these pathways and can lead to extracellular acidification via lactate.

Regulation of cancermetabolism involves oncogenic signaling networks, such as MYC, RAS, and PI3K/AKT/mTOR, as well as hypoxia-inducible factors. Tumor suppressors like p53 also influence metabolic choices. Metabolic plasticity allows cancer cells to adapt to nutrient scarcity, hypoxia, and therapeutic pressure, contributing to treatment resistance and disease progression.

Clinical relevance includes imaging applications, such as FDG-PET that detects heightened glucose uptake, and therapeutic approaches that target glycolysis, glutaminolysis, lipid synthesis, or mitochondrial function. These strategies aim to exploit cancer-specific metabolic vulnerabilities while minimizing effects on normal tissues.