The role of glycan-lectin interactions in the tumor microenvironment: immunosuppression regulators of colorectal cancer.

Abstract

Colorectal cancer (CRC) is a common malignant tumour and a serious global health issue. Glycosylation, a type of posttranslational modification, has been extensively studied in relation to cancer growth and metastasis. Aberrant glycosylation alters how the immune system in the microenvironment perceives the tumour and drives immune suppression through glycan-binding receptors. Interestingly, specific glycan signatures can be regarded as a new pattern of immune checkpoints. Lectins are a group of proteins that exhibit high affinity for glycosylation structures. Lectins and their ligands are found on endothelial cells (ECs), immune cells and tumour cells and play important roles in the tumour microenvironment (TME). In CRC, glycan-lectin interactions can accelerate immune evasion promoting the differentiation of tumour-associated M2 macrophages, altering T cell, dendritic cell (DC), natural killer (NK) cell, and regulatory T (Treg) cell activity to modify the functions of antigen-presenting cells functions. Here, we review our current knowledge on how glycan-lectin interactions affect immune-suppressive circuits in the TME and discuss their roles in the development of more effective immunotherapies for CRC.