Prostaglandin E2 and Interleukin-1β Reduce E-cadherin Expression by Enhancing Snail Expression in Gastric Cancer Cells

被引:11
|
作者
Jee, Ye Seob [2 ]
Jang, Tae Jung [1 ]
Jung, Ki Hoon [3 ]
机构
[1] Dongguk Univ, Coll Med, Dept Pathol, Gyeongju 780714, South Korea
[2] Dankook Univ Hosp, Dept Surg, Cheonan, South Korea
[3] Dongguk Univ, Coll Med, Dept Surg, Gyongju 780714, South Korea
关键词
Gastric cancer; Prostaglandin E-2; Interleukin-1; beta; E-cadherin; Snail; CYCLOOXYGENASE-2; EXPRESSION; MESENCHYMAL TRANSITION; PYLORI INFECTION; INFLAMMATION; PROGRESSION; ADHESION; LINES; HYPERMETHYLATION; INVASIVENESS; CARCINOMAS;
D O I
10.3346/jkms.2012.27.9.987
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Inflammation is closely related to the progression of cancer as well as tumorigenesis. Here, we investigated the effect of prostaglandin E-2 (PGE(2)) and interleukin-1 beta (IL-1 beta) on E-cadherin expression in SNU719 gastric cancer cells. E-cadherin expression decreased as the dose or exposure time of PGE(2) and IL-1 beta increased, whereas Snail expression increased with dose or time of PGE(2) and IL-1 beta. E-cadherin expression reduced by PGE(2) treatment increased after the transfection of Snail siRNA. Neutralization of IL-1 beta using anti-IL-1 beta antibody blocked the expression pattern of E-cadherin and Snail occurred by IL-1 beta treatment. However, there was no synergic effect of IL-1 beta and PGE(2) 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.
引用
收藏
页码:987 / 992
页数:6
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