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Beta-1,3- N -acetylglucosaminyltransferase 3 ( B3GNT3 ) has been associated with tumor progression in several solid tumors, and inhibits CD8 +  T cell-mediated anti-tumor immunity in breast cancer. However, little is known about the potential functions of  B3GNT3  in immunosuppression in pancreatic cancer (PC). This study on  B3GNT3  aims to provide novel insights into the mechanisms of immune suppression or evasion in PC. To this end, the clinical significance and oncologic roles of  B3GNT3  were investigated through bioinformatic analysis and  in vitro  studies. Potential associations between the expression of  B3GNT3  and tumor immunity were mainly analyzed by single-sample gene set enrichment analysis (ssGSEA) and immunofluorescence in tissue microarray (TMA).  B3GNT3  overexpression was observed in PC tissue and was associated with larger tumor sizes, higher histologic grades, and poorer overall survival (OS).  B3GNT3  overexpression was associated with the mutation status and expression of driver genes, especially for  KRAS  and  SMAD4 .  B3GNT3  knockdown inhibited the proliferation, invasion, and epithelial-mesenchymal transition (EMT) of PC cells.  B3GNT3  overexpression significantly correlated with decreased infiltration of tumor infiltrating lymphocytes (TILs), especially CD8 +  T cells. Overall, our results indicate that  B3GTN3  plays a novel role in tumor progression and immunosuppression, thus serving as a potential therapeutic target in PC.

B3GNT3 overexpression promotes tumor progression and inhibits infiltration of CD8+ T cells in pancreatic cancer