Positive relationship between p42.3 gene and inflammation in chronic non‐atrophic gastritis. Issue 10 (October 2015)

• Record Type: Journal Article
• Authors: Chen, Ping; Cui, Yun; Fu, Qing Yan; Lu, You Yong; Fang, Jing Yuan; Chen, Xiao Yu
• Is Part Of: Journal of digestive diseases. Volume 16:Issue 10(2015:Oct.)
• Page Start: 568
• Page End: 574
• Publication Date: 2015-10
• Subjects: gastritis -- Helicobacter pylori -- p42.3 -- stomach neoplasms, tumor necrosis factor‐alpha; Digestive organs -- Diseases -- Periodicals; Gastroenterology -- Periodicals; 616.3
• DOI: 10.1111/1751-2980.12282
• Languages: English
• ISSNs: 1751-2972

Abstract

Abstract : 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.