Galectin-3 and Epithelial MUC1 Mucin-Interactions Supporting Cancer Development

Simple Summary: MUC1 mucin with T antigen and galectin-3 with high affinity to T disaccharide are both overexpressed in a variety of human cancers. Their mutual interactions support cancer development, attenuate anoikis, promote cancer cells proliferation, invasiveness and metastasis. The inhibition of MUC1/T antigen-galectin-3 interactions may be a potential strategy to reduce tumor progression and metastasis. The aim of this review is to summarize the current knowledge about the relationship between MUC1 and galectin-3. Aberrant glycosylation of cell surface proteins is a very common feature of many cancers. One of the glycoproteins, which undergoes specific alterations in the glycosylation of tumor cells is epithelial MUC1 mucin, which is highly overexpressed in the malignant state. Such changes lead to the appearance of tumor associated carbohydrate antigens (TACAs) on MUC1, which are rarely seen in healthy cells. One of these structures is the Thomsen-Friedenreich disaccharide Gal beta 1-3GalNAc (T or TF antigen), which is typical for about 90% of cancers. It was revealed that increased expression of the T antigen has a big impact on promoting cancer progression and metastasis, among others, due to the interaction of this antigen with the beta-galactose binding protein galectin-3 (Gal-3). In this review, we summarize current information about the interactions between the T antigen on MUC1 mucin and Gal-3, and their impact on cancer progression and metastasis.