Cancer cells exhibit several unique metabolic features that distinguish them from normal cells. Cancer metabolism refers to these unique metabolic alterations as cells convert to a tumorigenic phenotype. These metabolic alterations are engaged both because of the oncogenic events that occur during cancer development and because tumour cells must adapt to a tumour microenvironment in which nutrients and oxygen are limited. One of the hallmark features of cancer metabolism is the Warburg effect, named after Otto Warburg. Cancer cells were found by Warburg to exhibit an increased dependence on glycolysis, the process of converting glucose into lactate, even under aerobic conditions (when oxygen is available). This preference for glycolysis, rather than oxidative phosphorylation, is now recognized as allowing cancer cells to generate biomass more efficiently, at the expense of energy generation to sustain their rapid proliferation. To sustain glycolysis, cancer cells exhibit enhanced glucose uptake and utilization. The resulting high rate of glucose consumption is a characteristic feature of cancer cells and is used in some imaging modalities. In concert, cancer cells often exhibit mitochondrial dysfunction and alterations in mitochondrial metabolism with decreased mitochondrial respiration and an increased reliance on glycolysis, even in the presence of oxygen. In addition to glucose, cancer cells exhibit increased uptake of amino acids, lipids, and other macromolecules to sustain anabolic processes such as protein and nucleic acid synthesis. This heightened demand for nutrients then supports their rapid proliferation. The pentose phosphate pathway (PPP), a metabolic pathway parallel to glycolysis, also plays a crucial role in cancer metabolism by helping to sustain anabolic processes in rapidly proliferating cancer cells. The PPP generates key molecules such as ribose-5-phosphate and NADPH, that are essential for nucleotide synthesis and antioxidant defence, respectively. Aside from glucose, glutamine - the most abundant amino acid nutrient in blood plasma - is also utilized by cancer cells to support various metabolic processes. Glutamine serves several functions required by cancer cells, serving as a carbon and nitrogen source for biosynthesis, contributing to the production of ATP, and providing intermediates for the tricarboxylic acid (TCA) cycle. Cancer cells often exhibit increased uptake and utilization of glutamine to sustain these metabolic demands. To increase tumour cell numbers, cancer cells must also make sufficient membrane lipids and, to do this frequently, exhibit alterations in lipid metabolism. They may enhance lipogenesis (de novo synthesis of fatty acids) to support membrane biogenesis and energy storage and can also increase lipid uptake, relying on exogenous fatty acids as a source of energy and membrane constituents. Cancer cells often experience elevated oxidative stress due to the increased production of reactive oxygen species (ROS) resulting from their metabolic alterations and rapid proliferation. To counteract ROS, which if left unchecked could result in cell death, cancer cells upregulate antioxidant defence mechanisms to maintain redox homeostasis, including increased production of reduced glutathione (GSH) and antioxidant enzymes. Finally, cancer cells must also support rapid DNA synthesis to increase cell numbers within the tumour microenvironment. Cancer cells can synthesize nucleotides de novo by converting amino acids, sugars, and carbon dioxide into nucleotides using ribonucleotide reductase and enzymes of the folate pathway. The salvage pathway and increased uptake of nucleosides are other important sources of nucleotides in rapidly proliferating cancer cells, either recycling nucleotide precursors from the breakdown of DNA and RNA or increasing uptake of nucleosides from the extracellular environment. Transporters on the cell membrane, such as equilibrative nucleoside transporters (ENTs) and concentrative nucleoside transporters (CNTs), facilitate the uptake of nucleosides from the surrounding tumour microenvironment. These nucleosides can be phosphorylated to form nucleotides for DNA synthesis. We offer a comprehensive product catalogue of research tools for investigating cancer metabolism, including Bcl-2 antibodies, Transferrin Receptor antibodies, GAPDH antibodies, Adiponectin ELISA Kits, and Myeloperoxidase ELISA Kits. Explore our full cancer metabolism product range below and discover more, for less. Alternatively, you can explore our Metabolic Signaling Pathway, Response to Hypoxia, and Cellular Metabolic Process product ranges.