Claudin and pancreatic cancer

Abstract

Due to the lack of timely and accurate screening modalities and treatments, most pancreatic cancer (PCa) patients undergo fatal PCa progression within a short period since diagnosis. The claudin(CLDN) family is expressed specifically as tight junction structure in a variety of tumors, including PCa, and affects tumor progression by changing the cell junctions. Thus far, many of the 27 members of the claudin family, including claudin-18.2 and claudin-4, have significantly aberrantly expression in pancreatic tumors. In addition, some studies have confirmed the role of some claudin proteins in the diagnosis and treatment of pancreatic tumors. By targeting different targets of claudin protein and combining chemotherapy, further enhance tumor cell necrosis and inhibit tumor invasion and metastasis. Claudins can either promote or inhibit the development of pancreatic cancer, which indicates that the diagnosis and treatment of different kinds of claudins require to consider different biological characteristics. This literature summarizes the functional characteristics and clinical applications of various claudin proteins in Pca cells, with a focus on claudin-18.2 and claudin-4.

Keywords: claudin (CLDN); claudin-18.2; claudin-4; diagnosis; pancreatic cancer (PCA); targeted therapy.

Figure 1

A schematic diagram of the claudin (CLDN) protein structure. Claudin has four transmembrane structures, a highly conserved extracellular loop (ECL)-1 sequence, a monoclonal antibody binding site (claudin-18.2), and serine/threonine/tyrosine kinase binding sites on the C-terminal. Claudin tail is inserted into the cell membrane after palmitoylation.