[Correlation of E-cadherin hypermethylation to tumorigenesis and development of gastric cancer]

Abstract

Background & objective: CpG island hypermethylation in promoter region of E-cadherin (E-cad) gene plays an important role in tumorigenesis of many tumors. This study was to explore the correlation of E-cadherin hypermethylation to tumorigenesis and development of gastric cancer.

Methods: Methylation-specific polymerase chain reaction (MSP) was used to detect the methylation of E-cad gene in 41 specimens of gastric cancer, 40 specimens of premalignant gastric lesions and 38 specimens of normal gastric tissues. The expression of E-cad protein was detected by SP immunohistochemistry.

Results: The positive rate of E-cad gene methylation was significantly higher in gastric cancer than in premalignant lesions and normal tissues (19.5% vs. 2.5% and 0.0%, P<0.05). The positive rate of E-cad protein was significantly lower in gastric cancer tissues than in premalignant lesions and normal tissues (70.7% vs. 97.5% and 100.0%, P<0.05). The positive rate of E-cad gene methylation was significantly higher in poorly differentiated cancer tissues than in well differentiated cancer tissues (43.8% vs. 4.0%, P<0.05), significantly higher in gastric cancer tissues with lymph node metastasis than in those without lymph node metastasis (33.3% vs. 5.0%, P<0.05), and significantly higher in gastric cancer tissues with serosa invasion than in those without serosa invasion (35.0% vs. 4.8%, P<0.05). The positive rate of E-cad protein was significantly lower in gastric cancer tissues with E-cad gene methylation than in those without E-cad gene methylation (0.0% vs. 87.9%, P<0.05).

Conclusion: CpG island hypermethylation of E-cad gene exists in gastric cancer, which down-regulates E-cad expression and might be involved in tumorigenesis and development of gastric cancer.