Helicobacter pylori Eradication Downregulates Cellular Inhibitor of Apoptosis Protein 2 in Gastric Carcinogenesis.
- Author:
Hyuk YOON
1
;
Sang Gyun KIM
;
Bo Kyoung KIM
;
Eun SHIN
;
Nayoung KIM
;
Hyuk Joon LEE
;
Gyeong Hoon KANG
;
Hyun Chae JUNG
Author Information
- Publication Type:Original Article
- Keywords: Helicobacter pylori; Cellular inhibitor of apoptosis protein 2; Gastric carcinogenesis
- MeSH: Apoptosis; Carcinogenesis*; Follow-Up Studies; Gastritis, Atrophic; Helicobacter pylori*; Helicobacter*; Humans; Inhibitor of Apoptosis Proteins*; Metaplasia; Real-Time Polymerase Chain Reaction; RNA, Messenger; Stomach Neoplasms
- From:Gut and Liver 2017;11(1):79-86
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/AIMS: To evaluate the expression of cellular inhibitor of apoptosis protein 2 (cIAP2) during gastric carcinogenesis after Helicobacter pylori (HP) infection and after HP eradication. METHODS: We divided non-cancer patients into four groups according to the status of HP infection and atrophic gastritis (AG)/intestinal metaplasia (IM). We compared cIAP2 mRNA expression among these four groups and patients with HP-positive early gastric cancer (EGC) by using real-time polymerase chain reaction (PCR). We evaluated the expression of cIAP2 messenger RNA (mRNA)/protein by using real-time PCR/immunohistochemistry and the degree of apoptosis with a terminal deoxynucleotidyl transferase-mediated nick end labeling assay before and 12 months after endoscopic submucosal dissection (ESD) in HP-positive EGC patients, regardless of whether they had undergone eradication therapy. RESULTS: The expression of cIAP2 mRNA was significantly higher in the groups with HP(+), AG/IM(+), and HP-positive EGC than in the control, HP(+), and AG/IM(−) groups (p<0.005). In the HP eradication group, the expression of cIAP2 mRNA/protein significantly decreased (p=0.006) and apoptosis increased at the 12-month follow-up after ESD. In the HP noneradication group, the aforementioned changes were not found during the same follow-up period. CONCLUSIONS: The expression of cIAP2 increased during gastric carcinogenesis after HP infection; HP eradication in the patients who had undergone ESD for EGC reversed overexpression of cIAP2 and suppressed cell apoptosis.
