Transcriptional control plays an important role in regulating cancer cell metabolism. Oncogenes and tumour suppressor genes (eg PI3K, PTEN) ultimately regulate transcriptional control, with oncogenes promoting cell growth and proliferation and tumour suppressor genes inhibit these processes. Mutations or dysregulation of these genes can lead to aberrant transcriptional control in cancer cells. In cancer cells alterations in the expression or activity of transcription factors can lead to upregulation or downregulation of metabolic genes. For example, transcription factor Myc is often overexpressed in cancer and regulates various aspects of cellular metabolism. Myc is known to promote both glucose uptake, glutamine metabolism, and lipogenesis thereby providing via one oncogenic change the building blocks necessary for tumour survival, growth and proliferation. Transcriptional control thereby directly impacts the expression of genes involved in cancer cell metabolism. Key metabolic pathways affected include glycolysis, the tricarboxylic acid (TCA) cycle, oxidative phosphorylation, fatty acid synthesis, and amino acid metabolism. Transcriptional changes in these genes can shift the cellular metabolism towards enhanced nutrient uptake, increased glycolysis (the Warburg effect), and altered utilization of metabolites. Epigenetic alterations, such as DNA methylation and histone modifications, can similarly profoundly affect transcriptional control in cancer cells. Hypermethylation of promoter regions can lead to the silencing of tumour suppressor genes involved in metabolic regulation, whilst hypomethylation may result in the activation of proto-oncogenes. Similarly, histone modifications can either promote or inhibit gene transcription, impacting cancer cell metabolism. Transcriptional control is also responsible for longer-term metabolic reprogramming of cancer cells. Reprogramming involves the upregulation of genes associated with glycolysis and the downregulation of oxidative phosphorylation genes, enabling cancer cells to survive and proliferate in a hypoxic, nutrient-limited environment. Transcriptional regulators such as hypoxia-inducible factors (HIFs) play a vital role in this process. Transcriptional control in cancer cell metabolism is also closely interconnected with signalling pathways frequently activated in cancer cells, such as PI3K/AKT, mTOR, and AMPK. Dysregulation of these pathways often leads to altered transcriptional activity, affecting the expression of multiple metabolic genes. For instance, activation of the PI3K/AKT pathway promotes the expression of both glucose transporters and glycolytic enzymes. Lipid biosynthesis, also critical for increased cancer cell proliferation, is proximally regulated by transcriptional regulation via the Peroxisome Proliferator-Activated Receptors (PPARs) pathway. PPARs are nuclear receptor transcription factors that regulate the expression of multiple genes collectively involved in lipid uptake, storage, and oxidation. They are activated in cells by fatty acids and their derivatives. Once activated, PPARs form heterodimers with retinoid X receptors (RXRs) and bind to specific DNA sequences to regulate gene expression. In addition, Sterol Regulatory Element-Binding Proteins (SREBPs) are transcription factors that similarly regulate lipid metabolism, including the synthesis of cholesterol and fatty acids. When cellular cholesterol levels are low, SREBP is activated. This pathway involves the proteolytic processing of SREBPs, subsequent translocation to the nucleus, and binding to specific target genes involved in lipid synthesis. Explore our full transcriptional control product range below and discover more, for less.