Positive relationship between p42.3 gene and inflammation in chronic non-atrophic gastritis
Positive relationship between p42.3 gene and inflammation in chronic non-atrophic gastritis
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p42.3基因与慢性非萎缩性胃炎炎症的正相关关系
DOI：
10.1111/1751-2980.12282
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发表时间：
2015-10-01
影响因子：
3.5
通讯作者：
Chen, Xiao Yu
中科院分区：
文献类型：
--
作者：
Chen, Ping;Cui, Yun;Chen, Xiao Yu
目的：胃癌是一种典型的炎症性肿瘤。P42.3基因在胃癌中高表达，但其与胃炎的关系尚不清楚。目的：探讨p42.3基因在体内外与胃炎症的关系。方法：用幽门螺杆菌和肿瘤坏死因子-α处理正常胃上皮细胞(GES-1)。提取并收集细胞总mRNA和蛋白，用聚合酶链式反应和Western印迹法检测p42.3基因的相对表达。共收集291例慢性非萎缩性胃炎患者活检标本，采用免疫组织化学方法检测p42.3蛋白的表达。结果：幽门螺杆菌和肿瘤坏死因子-α均能显著增强GES-1细胞p42.3蛋白的表达，并呈时间和剂量依赖关系。此外，p42.3基因表达与胃粘膜炎症程度、幽门螺杆菌感染呈正相关(P=0.000)。结论：p42.3基因表达与胃粘膜炎症有关，可被肿瘤坏死因子-α和幽门螺杆菌感染上调。
OBJECTIVE: Gastric cancer (GC) is a typical type of inflammation-related tumor. The p42.3 gene is shown to be highly expressed in GC, but its association with gastritis remains unknown. We aimed to explore the relationship between gastric inflammation and p42.3 gene in vitro and in vivo.METHODS: Normal gastric epithelial cells (GES-1) were treated with Helicobacter pylori (H. pylori) and tumor necrosis factor (TNF)-alpha. Total cell mRNA and protein were extracted and collected, and polymerase chain reaction and Western blot were performed to determine the relative expression of p42.3 gene. In total, 291 biopsy samples from patients with chronic non-atrophic gastritis were collected and immunohistochemistry was used to measure the p42.3 protein expression. The association between p42.3 protein expression and the clinicopathological characteristics of these patients were analyzed.RESULTS: Both H. pylori and TNF-alpha significantly enhanced the p42.3 protein expression in GES-1 cells in a time and dose-dependent manner. In addition, p42.3 gene expression was positively associated with the severity of gastric mucosal inflammation and H. pylori infection (P = 0.000). Its expression was significantly more common in severe gastric inflammation and in H. pylori-infected cases.CONCLUSION: p42.3 gene expression is associated with gastric mucosal inflammation that can be upregulated by TNF-alpha and H. pylori infection.