Ahcy, also known as adenosylhomocysteinase, is a highly conserved enzyme. It catalyzes the reversible breakdown of S-adenosylhomocysteine (SAH), a by-product and potent inhibitor of methyltransferases activity. This places Ahcy in the methionine cycle, which is crucial for cellular methylation levels. By removing excess SAH, Ahcy facilitates local transmethylation reactions, playing an essential role in DNA, RNA, and histone methylation during processes like replication and transcription [1].

In mouse and human adipocyte progenitor cells, inhibition of Ahcy using adenosine dialdehyde (AdOx) or siRNA-mediated knockdown reduces cell proliferation and number, as well as adipocyte differentiation and the expression of adipogenic markers. This indicates that Ahcy is necessary for the maintenance of these processes [2]. In colorectal cancer, loss of Apc in mouse intestine drives the expression of Ahcy, and targeting Ahcy function impairs the growth of APC-deficient organoids in vitro and prevents the characteristic hyperproliferative phenotype in vivo. Pharmacological inhibition of Ahcy also reduces intestinal tumour burden in ApcMin/+ mice, suggesting its potential as a metabolic drug target in CRC [3].

In conclusion, Ahcy is vital for maintaining normal cellular methylation levels and is essential for processes such as cell proliferation and differentiation. Mouse models, especially those with genetic alterations relevant to diseases like colorectal cancer, have revealed its potential as a therapeutic target in certain disease conditions, highlighting the importance of Ahcy in both normal biological functions and disease-related processes.