In colorectal cancer, lipid metabolism is a targetable metabolic vulnerability

Author(s): Erica Bronen

According to the World Health Organization, Colorectal Cancer (CRC) is the second biggest cause of cancer-related deaths. It is still a major public health issue around the world. Despite recent breakthroughs in early detection tests and treatment choices that have lowered CRC mortality in industrialised countries, the global incidence of CRC has been continuously rising. CRCs have recently been diagnosed in a growing proportion of people under the age of 50. The causes of this disturbing trend are unknown, but recent evidence suggests that dietary fat intake and obesity may be key contributors to the rising risk of early-onset CRC. Multiple investigations have shown the link between CRC and lipid changes, suggesting that lipid metabolism has a significant impact on the onset and course of CRC and is a targetable vulnerability in this illness. Fatty Acids (FAs), glycerolipids, glycerophospholipids, sphingolipids, sterol lipids, prenol lipids, saccharolipids, and polyketide are hydrophobic macromolecules divided into eight categories based on the presence of ketoacyl and isoprene groups. FAs are structural components of complex lipids that have numerous functions in the human body. FAs are crucial energy metabolism substrates, as well as necessary components for maintaining the structure and fluidity of all cell membranes. They also serve as building blocks for more structurally complex lipids. Lipids are involved in a variety of tasks, including signal transduction, intracellular trafficking, cell secretion, and motility, in addition to their role as energy substrates and structural components.