Galectins Are Central Mediators of Immune Escape in Pancreatic Ductal Adenocarcinoma

Simple Summary Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers with a high degree of immune tolerance. Galectins induce induction of immune evasion behavior in tumor cells. Galectins each play a role in promoting PDAC progression during PDAC immune evasion by coordinating the function and number of immune cells, especially galectin-1. In this paper. we review the involvement of galectins in the construction of PDAC privileged zones by regulating relevant immune cells, establishing fibrotic barriers, and promoting cellular metabolism. Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers and is highly immune tolerant. Although there is immune cell infiltration in PDAC tissues, most of the immune cells do not function properly and, therefore, the prognosis of PDAC is very poor. Galectins are carbohydrate-binding proteins that are intimately involved in the proliferation and metastasis of tumor cells and, in particular, play a crucial role in the immune evasion of tumor cells. Galectins induce abnormal functions and reduce numbers of tumor-associated macrophages (TAM), natural killer cells (NK), T cells and B cells. It further promotes fibrosis of tissues surrounding PDAC, enhances local cellular metabolism, and ultimately constructs tumor immune privileged areas to induce immune evasion behavior of tumor cells. Here, we summarize the respective mechanisms of action played by different Galectins in the process of immune escape from PDAC, focusing on the mechanism of action of Galectin-1. Galectins cause imbalance between tumor immunity and anti-tumor immunity by coordinating the function and number of immune cells, which leads to the development and progression of PDAC.

Automated summary

Pancreatic ductal adenocarcinoma (PDAC) is a highly immune-tolerant cancer. Galectins, particularly Galectin-1, play a crucial role in promoting PDAC progression by coordinating the function and number of immune cells. They induce abnormal functions and reduce numbers of tumor-associated macrophages, natural killer cells, T cells, and B cells. Galectins also promote fibrosis and enhance local cellular metabolism, ultimately constructing immune privileged areas for tumor cells. This review summarizes the mechanisms of different galectins, focusing on Galectin-1, in the immune escape of PDAC. The imbalance between tumor immunity and anti-tumor immunity caused by galectins leads to the development and progression of PDAC.