Ovarian cancer G-protein-coupled receptor 1 induces the expression of the pain mediator prostaglandin E2 in response to an acidic extracellular environment in human osteoblast-like cells

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• 作者：Juqiang Wang ; Yu Sun ; Hideaki Tomura ; Fumikazu Okajima
• 关键词：Bone pain ; Extracellular acidification ; Ovarian cancer G-protein-coupled receptor 1 ; Prostaglandin E2 ; MG63 cell
• 刊名：The International Journal of Biochemistry and Cell Biology
• 出版年：2012
• 出版时间：November, 2012
• 年：2012
• 卷：44
• 期：11
• 页码：1937-1941
• 全文大小：463 K

文摘

Although bone pain in osteoporosis and skeletal metastasis is an expected consequence of fracture, there are other underlying causes responsible. Our study demonstrated that ovarian cancer G-protein-coupled receptor 1 detected extracellular protons in MG63 cells, and regulated osteoblast functions, such as prostaglandin E2 production, in response to acidic circumstances. In this work, we measured inositol phosphate production, intracellular Ca²⁺ concentration, prostaglandin E2 production, and cyclic adenosine monophosphate accumulation in MG63 cells exposed to extracellular acidification. Extracellular acidity induced a transient increase in Ca²⁺ concentration and inositol phosphate production. Acidification also induced prostaglandin E2 production, resulting in cyclic adenosine monophosphate accumulation. A small interfering RNA specific for the ovarian cancer G-protein-coupled receptor 1 markedly inhibited these proton-induced actions in MG63 cells. These results indicated that the involvement of ovarian cancer G-protein-coupled receptor 1 in acidic extracellular environment may be an underlying mechanism responsible for bone pain in osteoporosis or bone metastasis without clinically proved fractures.