GLYAT, known as Glycine-N-acyltransferase, is an enzyme that catalyzes the transfer of acyl groups from acyl CoA to glycine, resulting in acyl glycine and coenzyme A. It is part of the phase II glycine conjugation pathway in the liver, which is crucial for maintaining adequate levels of free coenzyme A (CoASH) and detoxifying excess acyl-CoAs, such as benzoyl-CoA [3,4].

GLYAT has been shown to be lowly expressed in several cancers including liver cancer, clear cell renal cell carcinoma (ccRCC), and breast cancer. In liver cancer and ccRCC, overexpression of GLYAT inhibits cell proliferation and migration, and in vivo assays in nude mice confirm its tumor-suppressor function. It downregulates Rho-associated coiled-coil-containing protein kinase 1 (ROCK1), thus suppressing cancer progression [1]. In breast cancer, knockdown of GLYAT enhances cell proliferation and migration likely through activation of the PI3K/AKT/Snail pathway, which induces epithelial-mesenchymal transition (EMT) [2].

In conclusion, GLYAT plays a significant role in metabolic processes, especially in the glycine conjugation pathway for detoxification. Its downregulation is associated with tumor progression in multiple cancers, suggesting its potential as a prognostic biomarker and therapeutic target. The functional studies using in vivo models like nude mice have been instrumental in revealing its role in cancer-related biological processes [1,2].