Department of Pathology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Department of Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
Curr Med Sci. 2020 Feb;40(1):95-103. doi: 10.1007/s11596-020-2151-y. Epub 2020 Mar 13.
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 RELMβ expression in gastric carcinoma and precursor lesions. H. pylori infection and RELMβ expression were immunohistochemically evaluated in gastric biopsies from 230 patients. The biopsies consisted of normal gastric mucosa (n=20), mucosa with chronic gastritis (n=41), intestinal metaplasia (n=42), dysplasia (n=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 RELMβ expression was detected by reverse transcription PCR, real-time PCR and Western blotting. Higher RELMβ immunoreactivity was observed in H. pylori-positive 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 (P=0.005), 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 RELMβ intensity 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-ΔPAI) 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.
幽门螺杆菌（H. pylori）被报道与胃癌的发生有关。RELMβ是一种最近描述的杯状细胞特异性蛋白，在胃癌中异常表达，并与临床病理特征相关。本研究旨在探讨 H. pylori 与胃癌及其癌前病变中 RELMβ表达的关系。在 230 例患者的胃活检组织中，采用免疫组织化学方法检测 H. pylori 感染和 RELMβ的表达。活检组织包括正常胃黏膜（n=20）、慢性胃炎（n=41）、肠上皮化生（n=42）、异型增生（n=31）、肠型腺癌（n=56）和弥漫型腺癌（n=40）。在 32 例患者的 H. pylori 根除治疗后，测量了胃活检组织中 RELMβ的表达。用 H. pylori 菌株感染培养的胃癌细胞系 SGC-7901，通过逆转录 PCR、实时 PCR 和 Western blot 检测 RELMβ的表达。在 H. pylori 阳性的肠上皮化生（P=0.003）、异型增生（P=0.032）、肠型（P=0.037）和弥漫型腺癌（P=0.001）中，RELMβ的免疫反应性更高。RELMβ在异型增生（P=0.005）、肠型腺癌（P<0.001）和弥漫型腺癌（P=0.001）中的表达率与 H. pylori 密度的严重程度显著相关。此外，H. pylori 根除治疗可降低肠上皮化生（P=0.001）中 RELMβ的强度。胃癌 SGC-7901 细胞感染 cag 毒力岛（PAI）阳性 H. pylori TN2，但不感染其 PAI 完全缺失突变体（TN2-ΔPAI）4-8 小时后，RELMβ的蛋白和转录水平均增强（P<0.05）。综上所述，本研究表明，H. pylori 感染促进了胃癌及其癌前病变中 RELMβ的表达。
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