Figure 3.

Functional impact of STn and SLe^A expression in gastrointestinal tumors. Both STn and SLe^A overexpression influence tumor initiating processes as constitutive activation of several oncogenic signalling mediate by EGFR and ErbB2. Moreover, SLe^A also facilitates H. pylori adhesion to the gastric epithelium, contributing to persistent infection and potentially cancer development. STn also drives tumor progression by negatively impacting cell-cell and cell-extracellular matrix adhesion as well as galectin-3-mediated chemoresistance. Moreover, sialylated lewis antigens facilitate hematogenous metastasis of tumor cells through E-selectin interactions, while protecting tumor cells from sheer stress in circulation and hampering immune recognition.