前列腺素E受体EP4拮抗剂可抑制小鼠恶性黑色素瘤细胞骨转移所致的骨溶解。
Prostaglandin E receptor EP4 antagonist suppresses osteolysis due to bone metastasis of mouse malignant melanoma cells.
作者信息
Takita Morichika, Inada Masaki, Maruyama Takayuki, Miyaura Chisato
机构信息
Department of Biotechnology and Life Science, Tokyo University of Agriculture and Technology, 2-24-16 Nakamachi, Koganei, Tokyo 184-8588, Japan.
出版信息
FEBS Lett. 2007 Feb 6;581(3):565-71. doi: 10.1016/j.febslet.2007.01.005. Epub 2007 Jan 16.
We examined the effects of prostaglandin E (PGE) receptor subtype EP4 antagonist on bone metastasis of cancer to clarify PGE's role in bone metastasis. Metastatic regions were detected in femurs accompanying severe bone loss in mice injected with B16 malignant melanoma cells. Administration of EP4 antagonist restored the bone loss induced by B16 melanoma. Adding B16 cells induced osteoclast formation in the coculture of bone marrow cells and osteoblasts without any exogenous bone-resorbing factor, and EP4 antagonist completely suppressed the osteoclast formation induced by B16 cells. Therefore, EP4 antagonist is a possible candidate for the therapy of bone metastasis of cancer.
我们研究了前列腺素E（PGE）受体亚型EP4拮抗剂对癌症骨转移的影响，以阐明PGE在骨转移中的作用。在注射了B16恶性黑色素瘤细胞的小鼠股骨中检测到伴有严重骨质流失的转移区域。给予EP4拮抗剂可恢复由B16黑色素瘤诱导的骨质流失。在没有任何外源性骨吸收因子的情况下，添加B16细胞可诱导骨髓细胞和成骨细胞共培养体系中破骨细胞的形成，而EP4拮抗剂可完全抑制B16细胞诱导的破骨细胞形成。因此，EP4拮抗剂可能是治疗癌症骨转移的候选药物。
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