Abstract
Cyclooxygenase (COX)-2 and the prostaglandins resulting from its enzymatic activity have been shown to play a role in modulating cell growth and development of human neoplasia. Evidence includes a direct relationship between COX-2 expression and cancer incidence in humans and animal models, increased tumorigenesis after genetic manipulation of COX-2, and significant anti-tumor properties of non-steroidal anti-inflammatory drugs in animal models and in some human cancers. Recent data showed that COX-2 and the derived prostaglandins are involved in control of cellular growth, apoptosis, and signal through a group of nuclear receptors named peroxisome proliferator-activated receptors (PPARs). In this article we will review some of the findings suggesting that COX-2 is involved in multiple cellular mechanisms that lead to tumorigenesis.
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / metabolism
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Antineoplastic Agents / metabolism
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Apoptosis / physiology
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Cell Division / physiology*
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Cell Transformation, Neoplastic*
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Cyclooxygenase 2
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors / metabolism
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Gene Expression Regulation, Enzymologic
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Humans
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Isoenzymes / genetics
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Isoenzymes / metabolism*
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Membrane Proteins
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Prostaglandin-Endoperoxide Synthases / genetics
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Prostaglandin-Endoperoxide Synthases / metabolism*
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Prostaglandins / metabolism
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Receptors, Cytoplasmic and Nuclear / metabolism
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Transcription Factors / metabolism
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Antineoplastic Agents
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors
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Isoenzymes
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Membrane Proteins
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Prostaglandins
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Receptors, Cytoplasmic and Nuclear
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Transcription Factors
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Cyclooxygenase 2
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PTGS2 protein, human
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Prostaglandin-Endoperoxide Synthases