Abstract
We investigated the potential effect of Cyclooxygenase-2 (Cox-2) on hypoxia-induced Angiopoietin-2 (Ang-2) expression in gastric cancer cells. Our results revealed that hypoxia augmented Cox-2 and Ang-2 expressions. Also, the hypoxia-induced Ang-2 could be mimicked by CoCl(2) treatment while genestein treatment could partially counteract the hypoxia-induced Ang-2 expression. Celecoxib but not Cox-1 inhibitor sc-560 reversed the hypoxia-induced Ang-2 expression, while this effect could be partially restored by addition of exogenous PGE2. Our findings suggest that the hypoxia-elevated Ang-2 expression in gastric cancer cells may be mediated by both Cox-2-derived PGE2 and HIF-1alpha pathways, while celecoxib could counteract the hypoxia-induced Ang-2 expression.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Angiopoietin-2 / biosynthesis*
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Angiopoietins / metabolism
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology
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Celecoxib
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Cell Line, Tumor
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Cyclooxygenase 2 / biosynthesis*
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Cyclooxygenase Inhibitors / pharmacology*
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Dinoprostone / metabolism
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Gene Expression Regulation, Neoplastic*
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Humans
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Hypoxia*
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Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
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Pyrazoles / pharmacology*
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Reverse Transcriptase Polymerase Chain Reaction
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Stomach Neoplasms / metabolism*
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Sulfonamides / pharmacology*
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Up-Regulation*
Substances
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Angiopoietin-2
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Angiopoietins
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Anti-Inflammatory Agents, Non-Steroidal
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Cyclooxygenase Inhibitors
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HIF1A protein, human
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Hypoxia-Inducible Factor 1, alpha Subunit
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Pyrazoles
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Sulfonamides
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Cyclooxygenase 2
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Celecoxib
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Dinoprostone