Esophageal cancer (EC) is a unique and heterogeneous disease diagnosed mostly at advanced stages. Altered
glycans presented on cell surfaces are involved in the occurrence and development of
malignancy. However, the effects of
glycans on EC progression are largely unexplored. Here, a
lectin array was utilized to detect the
glycan profiling of the normal esophageal mucosal epithelial cell line and two EC cell lines. The binding of
Lens culinaris lectin (LCA) to EC cells was found to be stronger than that of the normal cells.
Lectin immunohistochemical staining revealed that LCA-binding
glycans were markedly elevated in EC tissues compared to adjacent non-cancerous tissues. LCA staining was significantly associated with
lymph node metastasis, depth of invasion, TNM stage and poor overall survival of EC patients. Added LCA to block LCA recognized
glycans could inhibit the migration and invasion of EC cells. Further analysis revealed that blocking the biosynthesis of LCA-binding
glycans by
tunicamycin attenuated cellular migratory and invasive abilities. Additionally, a
membrane glycoprotein CD147 was recognized as a binder of LCA. There was a positive correlation between LCA-binding
glycans and CD147 expression in clinical samples. Interestingly, CD147 inhibition also reduced cell migration and invasion. These findings indicated that LCA-binding
glycans may function as a novel
indicator to predict
metastasis for patients with EC.