Role of gene variants and E-cadherin localization in gastric mucosal cancerization.

BACKGROUND

This study investigates the role of gene single nucleotide polymorphisms (SNPs), mRNA transcription levels, and E-cadherin protein localization in Helicobacter pylori (Hp)-associated gastric diseases and their contribution to gastric mucosal carcinogenesis.

METHODS

Gastric mucosal samples were analyzed for histopathology (Hematoxylin-Eosin staining) and Hp detection (rapid urease test, Giemsa staining). SNPs at the gene rs16260 locus were identified via sequencing, mRNA levels were quantified by real-time PCR, and E-cadherin localization was assessed using Elivision™ Plus. Statistical analyses were performed with SPSS 25.0.

RESULTS

Participants were grouped by gastric mucosal pathology: normal (NOR), gastric inflammation (GI), gastric atrophy (GA), gastric premalignant lesion (GPL), severe dysplasia (GSD), and gastric cancer (GC). No significant differences were found in rs16260 genotypes. However, transcription was higher in GC compared to NOR and GPL groups. Intestinal metaplasia showed lower mRNA levels. E-cadherin expression was higher in GSD and GC compared to other groups. Localization analysis revealed decreased membrane-bound E-cadherin with increased cytoplasmic expression as lesion severity increased. Quantitative analysis showed higher E-cadherin expression in GA than other groups, indicating an initial rise followed by a decline in malignancy. Regression analysis suggested that elevated mRNA increased gastric cancer risk, while E-cadherin cytoplasmic ectopic expression heightened the risk of precancerous lesions and gastric cancer.

CONCLUSION

The A allele of the CDH1 gene rs16260 locus show no effect in gastric mucosal pathological evolution, while the elevated mRNA transcription levels potentially increasing the risk of gastric cancer. The loss and ectopic expression of E-cadherin may be significant risk factors for malignant transformation in the gastric mucosa.