LGALS3BP, also known as galectin 3-binding protein or 90K, is a multifunctional glycoprotein involved in various biological processes, including immunity and cancer. It is associated with several signaling pathways, such as the TGF-β1 signaling pathway, which is crucial in hepatic fibrosis and carcinogenesis [1].

In the context of hepatic diseases, LGALS3BP-knockout mice studies revealed that LGALS3BP deletion in hepatocytes downregulated TGF-β1 signaling and CCl4-induced fibrosis. LGALS3BP directly binds to and assembles integrin αV, releasing active TGF-β1, which activates JunB and promotes a TGF-β1 positive feedback loop. Thus, LGALS3BP depletion hindered hepatocarcinogenesis by limiting the availability of fibrogenic TGF-β1 [1].

In colon inflammation and tumorigenesis, Lgals3bp-/-mice were highly susceptible to colitis and colon tumorigenesis. Lgals3bp suppressed NF-κB through the downregulation of TAK1 in colon epithelial cells, indicating its role in suppressing colitis and colon tumorigenesis [2].

In conclusion, LGALS3BP plays essential roles in multiple biological processes and diseases. Its functions in hepatic fibrosis, hepatocarcinogenesis, colon inflammation, and tumorigenesis have been well-demonstrated through gene-knockout mouse models. These studies of LGALS3BP contribute to a better understanding of the disease mechanisms and may provide potential therapeutic targets for related diseases.