Cancer cells rewire their metabolism to support rapid growth, survival and spread. A central feature is altered glucose use. Many tumors show the Warburg effect: they preferentially ferment glucose to lactate even when oxygen is available, which seems inefficient but supports biosynthesis and signaling. This shift is driven by oncogenes such as MYC and RAS, loss of tumor suppressors like p53, and stabilization of HIF under low oxygen. These signals increase glucose uptake and glycolytic enzymes while reshaping downstream pathways.

Beyond glucose, cancer cells adjust amino acid and lipid metabolism. Glutamine becomes a key fuel and carbon source, feeding the tricarboxylic acid cycle and providing nitrogen for nucleotides and amino acids. Some tumors also rely heavily on serine and glycine metabolism and exploit one carbon pathways that generate building blocks and maintain redox balance. Lipid synthesis is often upregulated to produce membranes and signaling molecules, while fatty acid oxidation can be engaged to generate ATP and support survival under stress.

Metabolic changes are shaped by the tumor microenvironment. Regions of low oxygen and nutrients select for cells that can flexibly use alternative fuels, including lactate produced by neighboring cells. Interactions with stromal and immune cells further remodel metabolism. This complexity creates vulnerabilities. Therapies under study aim to inhibit key metabolic enzymes or transporters, restrict specific nutrients, or target the metabolic crosstalk between cancer and surrounding cells. However, the adaptability and diversity of tumor metabolism pose challenges, making context specific and combination strategies an active area of research.