Mboat2, short for membrane bound O-acyltransferase domain containing 2, is a phospholipid-modifying enzyme. It plays a crucial role in iron homeostasis by inhibiting iron sequestration, preventing iron-induced cell death through remodeling the phospholipid composition of cell membranes via phospholipid metabolism [5]. It is also transcriptionally upregulated by sex hormone receptors, like the androgen receptor [2].

In multiple cancer types, Mboat2 shows significant associations. In pancreatic cancer, its overexpression accelerates cell proliferation and migration, enhances CDK2 and CCNA2 expression for cell cycle progression, and reduces CD8+ T-cell infiltration [3]. In intrahepatic cholangiocarcinoma (ICC), a lipid-metabolism related circRNA, circMBOAT2, stabilizes PTBP1 to facilitate FASN mRNA cytoplasmic export, promoting ICC progression and lipid metabolism reprogramming [1]. In endometrial cancer, a five-gene metabolism-related risk signature including Mboat2 can predict prognosis and immune infiltration [4]. Also, MBOAT2 may act as a ferroptosis suppressor independent of GPX4 or FSP1 by remodeling the cellular phospholipid profile [2].

In conclusion, Mboat2 is involved in various biological processes, especially in lipid metabolism and iron homeostasis. Its dysregulation is closely related to the development of multiple cancers, highlighting its potential as a prognostic biomarker and a target for immunotherapy in malignancies. Research on Mboat2, including through gene knockout models (if applicable in the future), will further enhance our understanding of its role in disease mechanisms.