Prostaglandin E2 and Interleukin-1beta Reduce E-cadherin Expression by Enhancing Snail Expression in Gastric Cancer Cells.
10.3346/jkms.2012.27.9.987
- Author:
Ye Seob JEE
1
;
Tae Jung JANG
;
Ki Hoon JUNG
Author Information
1. Department of Surgery, Dankook University Hospital, Cheonan, Korea.
- Publication Type:Original Article
- Keywords:
Gastric cancer;
Prostaglandin E2;
Interleukin-1beta;
E-cadherin;
Snail
- MeSH:
Antibodies/immunology;
Antineoplastic Agents/pharmacology;
Cadherins/*metabolism;
Cell Line, Tumor;
Dinoprostone/*pharmacology;
Gene Expression Regulation/*drug effects;
Humans;
Interleukin-1beta/immunology/*pharmacology;
RNA Interference;
RNA, Small Interfering/metabolism;
Stomach Neoplasms/metabolism/pathology;
Transcription Factors/antagonists & inhibitors/genetics/*metabolism
- From:Journal of Korean Medical Science
2012;27(9):987-992
- CountryRepublic of Korea
- Language:English
-
Abstract:
Inflammation is closely related to the progression of cancer as well as tumorigenesis. Here, we investigated the effect of prostaglandin E2 (PGE2) and interleukin-1beta (IL-1beta) on E-cadherin expression in SNU719 gastric cancer cells. E-cadherin expression decreased as the dose or exposure time of PGE2 and IL-1beta increased, whereas Snail expression increased with dose or time of PGE2 and IL-1beta. E-cadherin expression reduced by PGE2 treatment increased after the transfection of Snail siRNA. Neutralization of IL-1beta using anti-IL-1beta antibody blocked the expression pattern of E-cadherin and Snail occurred by IL-1beta treatment. However, there was no synergic effect of IL-1beta and PGE2 on the expression pattern of E-cadherin and Snail. In conclusion, inflammatory mediators reduced E-cadherin expression by enhancing Snail expression in gastric cancer cells. Inflammation-induced transcriptional regulation of E-cadherin in gastric cancer has implications for targeted chemoprevention and therapy.
