Lpcat1, lysophosphatidylcholine acyltransferase 1, is a key enzyme in lipid remodeling, converting lysophosphatidylcholine into phosphatidylcholine. It is involved in the Lands cycle, regulating the fatty acyl chain composition of phospholipids in biological membranes [5]. This process impacts membrane biophysical properties, influencing various biological processes. Lpcat1 is crucial for proper lung function as it contributes to pulmonary surfactant biosynthesis [5].

In multiple diseases, Lpcat1 shows significant impacts. In cancer, Lpcat1 has been implicated in promoting tumor growth and metastasis. For instance, in esophageal squamous cell carcinoma, Lpcat1 reprograms cholesterol metabolism, promoting cancer progression [1]. In lung adenocarcinoma, it promotes brain metastasis by up-regulating the PI3K/AKT/MYC pathway [2]. In hepatocellular carcinoma, its overexpression correlates with poor prognosis and fuels cancer progression [6]. In cutaneous squamous cell carcinoma, Lpcat1 contributes to cancer development via EGFR-mediated signaling pathways [7]. In psoriasis, Lpcat1 facilitates keratinocyte hyperproliferation and skin inflammation by regulating GLUT3 [3]. In melanoma, it promotes cell proliferation through the Akt signaling pathway [4].

In conclusion, Lpcat1 plays essential roles in lipid remodeling and pulmonary function. Its dysregulation in various diseases, especially cancer, psoriasis, and melanoma, has been revealed through in vivo and in vitro studies. These findings suggest that Lpcat1 could potentially be a therapeutic target for these diseases, highlighting the importance of further research on its functions and mechanisms.