Abstract
Epidemiological data suggest that Non Steroidal Anti Inflammatory Drugs (NSAIDs) and Cyclooxygenase 2 (COX2) inhibitors (COXibs) can exert chemopreventive and antitumour effects in many human neoplasia. This is particularly true in colon cancer (CC), where the regular assumption of these molecules has been shown to exert chemopreventive and chemotherapeutic effects. Since the late '90s, there has been a progressive increase in experimental evidence, indicating that in CC the antiproliferative effects of NSAIDs and COXibs could be both dependent on and independent of COXs inhibition, and that these effects do not necessarily exclude each other. This review will examine some of these COX-independent cellular pathways, with a focus on those involved in the inhibition of CC cells proliferation through transcription factors crosstalk.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Anticarcinogenic Agents / therapeutic use*
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Cell Cycle / drug effects
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / metabolism
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Cell Proliferation / drug effects
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Cell Transformation, Neoplastic / drug effects*
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / metabolism
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Cell Transformation, Neoplastic / pathology
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Cyclooxygenase Inhibitors / therapeutic use*
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Gene Expression Regulation, Neoplastic
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Humans
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Inflammation / genetics
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Inflammation / metabolism
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Inflammation / pathology
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Inflammation / prevention & control*
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Inflammation Mediators / metabolism
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Neoplasms / enzymology
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Neoplasms / genetics
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Neoplasms / pathology
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Neoplasms / prevention & control*
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Risk Factors
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Signal Transduction / drug effects
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Transcription Factors / genetics
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Transcription Factors / metabolism
Substances
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Anticarcinogenic Agents
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Cell Cycle Proteins
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Cyclooxygenase Inhibitors
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Inflammation Mediators
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Transcription Factors