Expression of the E-cadherin/β-catenin/tcf-4 Pathway in Gastric Diseases with Relation to Helicobacter pylori Infection: Clinical and Pathological Implications


Objective: To determine the expression of E-cadherin, β-catenin, and transcription factor 4 (TCF4) proteinsin gastric diseases with relation to Helicobacter pylori infection.
Methods: A total of 309 patients including 60 withsuperficial gastritis (SG), 57 with atrophic gastritis (AG) and 192 with gastric cancer (GC), were enrolled. Theexpression of E-cadherin, β-catenin, TCF4 proteins in the gastric mucosa was detected by immunohistochemistryand H. pylori infection by immunohistochemistry and PCR.
Results: The expression rates of E-cadherin weresignificantly higher in SG and AG than in GC (P<0.01), while those of β-catenin in the nucleus were significantlylower in SG and AG than in GC (P<0.05). In GC cases, the expression rates of E-cadherin, β-catenin and TCF4were significantly higher in the intestinal type than in the diffuse type (P<0.05). In GC patients, the expressionrate of E-cadherin was significantly higher in the presence of H. pylori than in the absence of infection (P=0.011).Moreover, the expression level of TCF4 and β-catenin protein was significantly higher in the nucleus and cytoplasmin H. pylori positive than in H. pylori negative GC patients, especially in those with the intestinal type (all P <0.05).
Conclusion: The expression of E-cadherin and β-catenin progressively decreases during the process of GCtumorigenesis, while overexpression of TCF4 occurs. H. pylori infection is associated with a significant increasein the expression of E-cadherin and β-catenin in the cytoplasm and nucleus in GC patients, especially those withthe intestinal type.