Abstract
Prostaglandin E(2) is a crucial mediator to maintain physiological homeostasis and several disease progression. In this article, we summarized the roles of PGE(2) in bone resorptive metastatic model using B16 melanoma. An antagonist of EP4, a receptor subtype for PGE(2), suppressed RANKL expression in osteoblast and following osteoclast formation that was induced by B16, suggesting cancer induced bone resorption mediate PGE(2) production in host osteoblast is a key role of cancer metastasis to bone.
MeSH terms
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Animals
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Bone Neoplasms / etiology*
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Bone Neoplasms / secondary*
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Bone Resorption / etiology
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Dinoprostone / biosynthesis
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Dinoprostone / physiology*
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Disease Progression
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Homeostasis
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Humans
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Melanoma, Experimental
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Osteoblasts / metabolism
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Osteoclasts
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RANK Ligand / metabolism
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Receptors, Prostaglandin E / antagonists & inhibitors
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Receptors, Prostaglandin E, EP4 Subtype
Substances
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PTGER4 protein, human
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RANK Ligand
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Receptors, Prostaglandin E
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Receptors, Prostaglandin E, EP4 Subtype
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Dinoprostone