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KMID : 0811720100140030139
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Korean Journal of Physiology & Pharmacology
2010 Volume.14 No. 3 p.139 ~ p.144
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Redox Factor-1 Inhibits Cyclooxygenase-2 Expression via Inhibiting of p38 MAPK in the A549 Cells
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Yoo Dae-Goon
Kim Cuk-Seong
Lee Sang-Ki
Kim Hyo-Shin
Cho Eun-Jung
Park Myoung-Soo
Lee Sang-Do
Park Jin-Bong
Jeon Byeong-Hwa
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Abstract
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In this study, we evaluated the role of apurinic/apyrimidinic endonuclease1/redox factor-1 (Ref-1) on the tumor necrosis factor-? (TNF-?) induced cyclooxygenase-2 (COX-2) expression using A549 lung adenocarcinoma cells. TNF-? induced the expression of COX-2 in A549 cells, but did not induce BEAS-2B expression. The expression of COX-2 in A549 cells was TNF-? dose-dependent (5∼100 ng/ml). TNF-?-stimulated A549 cells evidenced increased Ref-1 expression in a dose-dependent manner. The adenoviral transfection of cells with AdRef-1 inhibited TNF-?-induced COX-2 expression relative to that seen in the control cells (Ad?gal). Pretreatment with 10?M of SB203580 suppressed TNF-?- induced COX-2 expression, thereby suggesting that p38 MAPK might be involved in COX-2 expression in A549 cells. The phosphorylation of p38 MAPK was increased significantly after 5 minutes of treatment with TNF-?, reaching a maximum level at 10 min which persisted for up to 60 min. However, p38MAPK phosphorylation was markedly suppressed in the Ref-1-overexpressed A549 cells. Taken together, our results appear to indicate that Ref-1 negatively regulates COX-2 expression in response to cytokine stimulation via the inhibition of p38 MAPK phosphorylation. In the lung cancer cell lines, Ref-1 may be involved as an important negative regulator of inflammatory gene expression.
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KEYWORD
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Redox factor-1, Cyclooxygenase-2, A549, Lung cancer, p38 MAPK
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