Abstract
Colorectal cancer poses a major clinical challenge in the developed world where this disease is common. Recent findings suggest that the prostaglandin E(2), the proinflammatory product of elevated cyclooxygenase-2 activity in colon cancer, stimulates cancer cell growth through a G protein-dependent signaling pathway coupling the prostaglandin EP2 receptor to beta-catenin control. These findings provide new insights into the molecular framework needed to evaluate chemopreventive strategies for colorectal cancer.
Publication types
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Research Support, N.I.H., Intramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Colorectal Neoplasms / metabolism
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Colorectal Neoplasms / physiopathology
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Colorectal Neoplasms / prevention & control*
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Cyclooxygenase 2 / metabolism*
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Cyclooxygenase 2 Inhibitors / therapeutic use*
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Dinoprostone / metabolism
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GTP-Binding Proteins / metabolism
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Humans
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Models, Biological
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Receptors, Prostaglandin E / physiology
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Receptors, Prostaglandin E, EP2 Subtype
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Signal Transduction / physiology
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beta Catenin / physiology
Substances
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Cyclooxygenase 2 Inhibitors
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PTGER2 protein, human
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Receptors, Prostaglandin E
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Receptors, Prostaglandin E, EP2 Subtype
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beta Catenin
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Cyclooxygenase 2
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GTP-Binding Proteins
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Dinoprostone