LAUSR

One carbon (1C) unit metabolism plays a central role in supporting cell growth and proliferation in the body through the perception of cell glucose, amino acid and other nutritional statuses. The 1C metabolism pathway provides cellular components, including nucleotides, lipids, and proteins, for cell growth via folic acid and methionine cycles. The 1C metabolism pathway also generates glutathione and S-adenosylmethionine to maintain cellular redox status and epigenetic status with cytosolic or mitochondrial folate metabolism. Targeting 1C unit metabolic enzymes and downstream nucleic acid metabolic enzymes is seen as a viable cancer treatment method since the metabolism of amino acids (such as serine and glycine) and the 1C units they provide are suf fi cient to promote tumor growth [1]. Mitochondrial 1C ux consistently overexpressed in cancer and supplied by the folic acid cycle and the mitochondrial serine-hydroxymethyltransferase (SHMT2), while cytosolic 1C fl ux is induced by the cytosolic enzyme SHMT1. Mitochondrial and cytosolic 1C fl ux is responsible for DNA replication and methylation. However, several studies that blocking mitochondrial 1C fl ux with SHMT2 inhibitors cannot abolish the neoplasia of hepatocellular cancer cells