Fgl1, short for Fibrinogen-like protein 1, is a protein secreted by the liver. It is involved in multiple biological functions such as promoting hepatocyte growth, regulating lipid metabolism, and influencing the tumor microenvironment. It is also related to the regulation of hepcidin and iron metabolism, and is a ligand of lymphocyte activation gene 3 (LAG3), playing a role in immune-related pathways [1,3,5,7].

In metastatic colorectal cancer, Fgl1 secreted from cancer cells and hepatocytes facilitates tumor progression by reducing T-cell infiltration. Tumor-associated macrophages (TAMs) in the liver microenvironment upregulate Fgl1 stability. Disrupting the TAM-OTUD1-Fgl1 axis can inhibit metastatic tumor progression [2]. In non-small cell lung cancer, high Fgl1 expression confers gefitinib resistance by regulating the PARP1/caspase 3 pathway, and it also promotes tumor progression and metastasis through the KDM4A/STAT3 transcription mechanism. Additionally, in Systemic lupus erythematosus, the Fgl1-LAG3 axis impairs the suppressive function of regulatory T cells [4,6,8].

In conclusion, Fgl1 has diverse biological functions. Its role in diseases like cancer, iron metabolism-related disorders, and autoimmune diseases has been revealed through various studies. These findings from different disease models, especially those related to cancer, highlight Fgl1 as a potential therapeutic target and biomarker, which is crucial for developing new strategies for disease treatment and prevention.