It is now widely recognized that altered metabolism is a hallmark of cancer cells and plays a critical role in tumour development, progression, and responses to therapy. The Warburg effect is one such hallmark and refers to the tendency of cancer cells to preferentially utilize glycolysis for energy production, even in the presence of oxygen (aerobic glycolysis). Aerobic glycolysis leads to the production of lactate, with the fate of lactate varying depending on the tumour microenvironment and the type of cancer. Lactate is actively exported out of the cancer cells and into the extracellular space via monocarboxylate transporters (MCTs). Extracellular lactate accumulation however creates an acidic microenvironment around the tumour, which can promote tumour progression and invasion. Lactate released by cancer cells can also be utilized by tumour-promoting cancer-associated fibroblasts or immune cells. These cells can convert lactate back into pyruvate, which can then be used for their own biosynthetic pathways. Some cancer cells can also re-import lactate back into their cytoplasm and mitochondria. Once inside the cell, lactate can be converted back to pyruvate by lactate dehydrogenase (LDH) and used in various metabolic pathways to support the energy demands and biosynthesis of cancer cells. Whilst less efficient in terms of ATP production compared to oxidative phosphorylation, the Warburg effect thereby allows cancer cells to rapidly generate energy and, critically, generate biosynthetic precursors, which are needed for their rapid proliferation. Cancer cells also exhibit increased glucose uptake and glycolysis, facilitated by overexpression of both glucose transporters (e.g., GLUT1) and glycolytic enzymes. The upregulation of key glycolytic enzymes, such as hexokinase and pyruvate kinase, further supports the Warburg effect with the metabolic shift towards increased glucose utilization providing cancer cells with a survival and biosynthetic advantage. In addition to alterations in glucose metabolism, cancer cells often display changes in lipid and amino acid metabolism. Lipids are essential for both new membrane synthesis and for functions in cellular signalling. Cancer cells frequently enhance de novo lipid synthesis and upregulate fatty acid uptake and storage to meet their high demand for membrane building blocks and energy substrates. Amino acid metabolism is also rewired in cancer cells. Certain amino acids, such as glutamine and serine, become critical for some cancer cells to survive and proliferate. Glutamine is utilized for energy production and serves as a precursor for nucleotide and amino acid synthesis, whilst serine metabolism is involved in nucleotide synthesis and redox balance, both crucial for cancer cell proliferation. Many cancer cells exhibit altered mitochondrial function, with some cancers showing reduced mitochondrial mass and oxidative phosphorylation capacity. Such mitochondrial dysfunction contributes to the Warburg effect and promotes cancer cell survival under hypoxic conditions. Finally, metabolic interactions between cancer cells and their surrounding microenvironment also plays a significant role in tumour progression. Cancer-associated fibroblasts (CAFs) and immune cells can undergo metabolic reprogramming to support cancer cell growth and survival. Metabolic crosstalk between cancer and stromal cells is thereby thought to influence tumour invasion, angiogenesis, and immune evasion. We offer a large product catalogue of research tools for investigating cancer, including Bcl-2 antibodies, Transferrin Receptor antibodies, GAPDH antibodies, Leptin ELISA Kits, and Insulin ELISA Kits. Explore our full cancer product range below and discover more, for less.