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COX-2 is essential for EGF induction of cell proliferation in gastric RGM1 cells.

Abstract：

:Growth factors upregulate cyclooxygenase-2 (COX-2) expression and extracellular signal-regulated kinase (ERK) activity, yet little is known regarding the interaction between COX-2 and ERK in terms of mitogenic signal transduction pathways in gastric epithelial cells. Therefore, we examined the role of COX-2 in EGF-induced proliferation of gastric epithelial RGM1 cells. EGF treatment significantly induced ERK activity (peaked at 30 min) and significantly increased COX-2 protein (peaked at 6 hr), production of prostaglandin E2 (PGE2), and cell proliferation. MEK inhibitor (PD98059) decreased ERK activity and cell proliferation induced by EGF. The selective COX-2 inhibitor (NS-398) significantly reduced EGF-induced cell proliferation. Exogenous PGE2 partly reversed the NS-398-induced inhibitory action on cell proliferation, clearly indicating the importance of PGE2 in mitogenic pathway. The induction of COX-2 protein by EGF was completely blocked by preincubation with MEK inhibitor. These results suggest that the ERK-COX-2 pathway is critical for EGF-induced proliferation of gastric epithelial cells.

journal_name

Dig Dis Sci

journal_title

Digestive diseases and sciences

authors

Sasaki E,Tominaga K,Watanabe T,Fujiwara Y,Oshitani N,Matsumoto T,Higuchi K,Tarnawski AS,Arakawa T

doi

10.1023/b:ddas.0000007860.87503.09

subject

Has Abstract

pub_date

2003-12-01 00:00:00

pages

2257-62

issue

12

eissn

0163-2116

issn

1573-2568

journal_volume

48

pub_type

杂志文章

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