Helicobacter pylori Infection Facilitates the Expression of Resistin-like Molecule Beta in Gastric Carcinoma and Precursor Lesions

摘要

Helicobacter pylori(H.pylori)was reported to be associated with gastric carcinogenesis.Resistin-like molecule beta(RELMβ),a recently described goblet cell-specific protein,was demonstrated to aberrantly express in gastric cancer and correlated with its clinicopathological features.This study aimed to examine the association between H.pylori and RELMp expression in gastric carcinoma and precursor lesions.H.pylori infection and RELMβexpression were immunohistochemically evaluated in gastric biopsies from 230 patients.The biopsies consisted of normal gastric mucosa(w=20),mucosa with chronic gastritis(n=41),intestinal metaplasia(n=42),dysplasia(w=31),intestinal-type adenocarcinoma(n=56),and diffuse-type adenocarcinoma(n=40).RELMβ expression was measured in gastric biopsies after H.pylori eradication therapy in a subgroup of 32 patients.Cultured gastric cancer cell line SGC-7901 was infected with H.pylori strains,and RELMp expression was detected by reverse transcription PCR,real-time PCR and Western blotting.Higher RELMP immunoreactivity was observed in H.pyloripositive intestinal metaplasia(P=0.003),dysplasia(P=0.032),intestinal-type(P=0.037)and diffuse-type adenocarcinomas(P=0.001)than in H.pylori-negative specimens.Expression rates of RELMβ in dysplasia(CO.005),intestinal-type adenocarcinoma(P<0.001),and diffuse-type adenocarcinoma(P=0.001)were significantly correlated with the grade of H.pylori density.In addition,H.pylori eradication reduced the RELMβintensity in intestinal metaplasia(P=0.001).Infection of gastric cancer SGC-7901 cells with cag pathogenicity island(PAI)-positive H.pylori TN2,but not with its PAI totally deleted mutant(TN2-APAI)for 4-8 h,resulted in enhanced protein and transcript levels of RELMβ(P<0.05).In summary,our study suggested that H.pylori infection facilitated the expression of RELMβ in gastric garcinoma and precursor lesions.