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Positive relationship between p42.3 gene and inflammation in chronic non‐atrophic gastritis
Author(s) -
Chen Ping,
Cui Yun,
Fu Qing Yan,
Lu You Yong,
Fang Jing Yuan,
Chen Xiao Yu
Publication year - 2015
Publication title -
journal of digestive diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 51
eISSN - 1751-2980
pISSN - 1751-2972
DOI - 10.1111/1751-2980.12282
Subject(s) - inflammation , helicobacter pylori , gastritis , medicine , immunohistochemistry , tumor necrosis factor alpha , atrophic gastritis , biopsy , western blot , pathology , cancer , gastric mucosa , downregulation and upregulation , gene expression , stomach , gastroenterology , gene , biology , biochemistry
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)‐α. 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‐α 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‐α and H. pylori infection.