Figure 6.

Schematic illustration depicting the putative interactions between MUC1, β-catenin, and CagA in H. pylori-infected gastric epithelial cells. (A) Without MUC1 over-expression, CagA delivered to the cytosol of H. pylori (Hp)-infected cells displaces β-catenin (β) from E-cadherin (E-cad), allowing β-catenin to translocate to the nucleus and activate IL-8 gene expression. (B) With MUC1 over-expression, β-catenin that is displaced by CagA binds to MUC1 (i), thus blocking its nuclear translocation and attenuating IL-8 production. CagA also binds to MUC1, possibly either without (ii) or with (iii) β-catenin.