RUNX3 Methylation, Loss of RUNX3 Expression and Clinicopathologic Findings according to Helicobacter pylori CagA in Gastric Carcinoma.
- Author:
Yoon Ju NA
1
;
Ki Nam SHIM
;
Yang Hee JOO
;
Seong Eun KIM
;
Hye Kyung JUNG
;
Sung Ae JUNG
;
Min Sun CHO
Author Information
- Publication Type:Original Article
- Keywords: Helicobacter pylori; CagA; RUNX3; Methylation; Carcinoma
- MeSH: Adult; Aged; Aged, 80 and over; Antigens, Bacterial/*metabolism; Bacterial Proteins/*metabolism; Cell Line, Tumor; Core Binding Factor Alpha 3 Subunit/genetics/*metabolism; Female; *Gene Expression Regulation, Neoplastic; Helicobacter Infections/complications/microbiology; Helicobacter pylori/isolation & purification/*metabolism; Humans; Immunohistochemistry; Lymphatic Metastasis; Male; Methylation; Middle Aged; Neoplasm Staging; Promoter Regions, Genetic; Retrospective Studies; Stomach Neoplasms/complications/microbiology/*pathology
- From:The Korean Journal of Gastroenterology 2015;66(2):75-84
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/AIMS: Helicobacter pylori cytotoxin-associated gene A (CagA) has been suggested to be involved in the inactivation of Runt-related transcription factor 3 (RUNX3), a known gastric carcinoma tumor suppressor gene. It remains unclear how H. pylori CagA initiates or maintains RUNX3 promoter methylation and inactivates its protein expression in gastric carcinoma. METHODS: RUNX3 promoter methylation status, RUNX3 expression, and H. pylori CagA were investigated in 76 sample pairs of gastric carcinoma tissue. The patients' medical records were reviewed. The association between RUNX3 methylation or loss of RUNX3 expression and clinicopathologic variables according to H. pylori CagA status were investigated. RESULTS: In gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation did not show association with lymphatic invasion, venous invasion, and TNM stages. However RUNX3 methylation was observed more frequently in poorly differentiated adenocarcinoma and signet ring cell carcinoma (77.8% vs. 20.0%, p=0.023) in early stage. In gastric carcinoma patients with H. pylori CagA-positive infection, loss of RUNX3 expression did not show association with lymphatic invasion, venous invasion, and TNM stages. However loss of RUNX3 expression was observed more frequently in early gastric carcinoma than in advanced gastric carcinoma (84.2% vs. 75.0%, p=0.51), but this difference was not significant. CONCLUSIONS: In gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation or loss of RUNX3 expression did not show correlation with lymphovascular invasion and TNM stages. In early gastric carcinoma patients with H. pylori CagA-positive infection, RUNX3 methylation was observed more in poorly differentiated adenocarcinoma and signet ring cell carcinoma.
