St3gal4, also known as ST3 beta-galactoside alpha-2,3-sialyltransferase 4, is a sialyltransferase enzyme. It plays a crucial role in regulating biological processes by modifying glycoproteins through sialylation. It is involved in multiple pathways such as receptor protein tyrosine kinase terminal glycan sialylation, which impacts cell-signaling related to growth and survival. Its biological importance spans across various aspects of cell function and is relevant in disease development [1,2,3,4,5,6,7,8].

In non-small cell lung cancer, knockdown of St3gal4 resensitizes resistant cells to osimertinib, indicating its role in conferring drug resistance [1]. In breast cancer, inhibiting St3gal4 expression decreases cell viability, disrupts cell cycle progression, and reduces aerobic glycolysis, suggesting its role in promoting tumorigenesis [2]. In glioma, knockdown of St3gal4 reduces cell line proliferation, migration, and invasion, while causing G1 phase cell cycle arrest [3]. In acute myeloid leukemia, depletion of St3gal4 by CRISPR-Cas9 knockout enhances the sensitivity of AML cells to phagocytosis by Siglec-9-expressing macrophages, revealing its role in immune evasion [4]. In osteosarcoma, knockdown of St3gal4 significantly inhibits proliferation, migration, invasion, and glycolysis of osteosarcoma cells and inhibits the M2 polarization of macrophages [6]. In influenza virus research, knockout of St3gal4 prevents the adsorption of swine and avian influenza viruses [7].

In conclusion, St3gal4 is a key enzyme in sialylation-mediated biological functions. Through gene-knockout studies in various disease models, it has been shown to play significant roles in drug resistance in non-small cell lung cancer, tumorigenesis in breast cancer, glioma malignancy, immune evasion in acute myeloid leukemia, and the progression and immune microenvironment of osteosarcoma, as well as influenza virus adsorption. These findings highlight its potential as a therapeutic target in multiple disease areas.