Ezrin and Radixin Differentially Modulate Cell Surface Expression of Programmed Death Ligand-1 in Human Pancreatic Ductal Adenocarcinoma KP-2 Cells

Immune checkpoint blockade (ICB) therapies, such as immune inhibitors against programmed death ligand-1 (PD-L1), have not been successful in treating patients with pancreatic ductal adenocarcinoma (PDAC). Despite the critical role of PD-L1 various types cancers, regulatory mechanism expression on cell surface PDAC is poorly understood. Therefore, uncovering potential modulators localisation may provide a new strategy to improve ICB therapy PDAC. Here, we examined ezrin/radixin/moesin (ERM) family scaffold proteins that crosslink transmembrane actin cytoskeleton KP-2 cells, human line. Our results demonstrated abundant protein PD-L1, ezrin, and radixin, but moesin, well their colocalisation plasma membrane. Interestingly, immunoprecipitation analysis detected molecular interaction ezrin radixin. Moreover, gene silencing moderately decreased mRNA while radixin greatly without altering levels. Thus, differentially modulate highlighting therapeutic target current