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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >The effect of cyclooxygenase-2 (COX-2) inhibition on human prostate cancer induced osteoblastic and osteolytic lesions in bone.
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The effect of cyclooxygenase-2 (COX-2) inhibition on human prostate cancer induced osteoblastic and osteolytic lesions in bone.

机译：环氧合酶2（COX-2）抑制对人前列腺癌诱导的骨成骨和溶骨性病变的影响。

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BACKGROUND: The mechanism of bone formation by osteoblastic prostate cancer metastases is not well defined. Using knockout mice, it has been demonstrated that prostaglandins produced by COX-2 are critical for fracture repair. Therefore, our aim was to determine if COX-2 plays a role in the bone formation in osteoblastic prostate cancer metastases in bone. MATERIALS AND METHODS: We assessed the influence of pharmacologic COX-2 inhibition in a SCID mouse intratibial injection model of bone metastasis using two human prostate cancer cell lines that produce either osteoblastic lesions (LAPC-9) or osteolytic lesions (PC-3, negative control). SC-58236, a COX-2 specific inhibitor, was used at a dose of 3 mg/Kg intraperitoneally 3 times per week in the Treatment groups for 8 weeks until sacrifice. RESULTS: Western blot for COX-2 demonstrated that LAPC-9 cells expressed high levels of COX-2 while PC-3 cells did not. Treatment with SC-58236 significantly reduced the size of osteoblastic lesions after LAPC-9 injection based on both radiographic and histomorphometric criteria compared to the control group. In contrast, large osteolytic lesions were seen in both control and SC-58236 treated animals after PC-3 cell injections. The results of this study indicate that COX-2 inhibition can decrease the size of osteoblastic lesions produced by LAPC-9, a human prostate cancer cell line that expresses high levels of COX-2. This treatment had no effect on the osteolytic activity of PC-3 cells. CONCLUSION: These findings suggest that the progression of osteoblastic metastases induced by human prostate cancer cells may be limited by COX-2 inhibitors.
机译：背景：成骨细胞前列腺癌转移的骨形成机制尚未明确。使用敲除小鼠，已证明由COX-2产生的前列腺素对于骨折修复至关重要。因此，我们的目的是确定COX-2是否在骨成骨性前列腺癌转移中的骨形成中起作用。材料和方法：我们使用两种人类前列腺癌细胞系（产生成骨性病变（LAPC-9）或溶骨性病变（PC-3，阴性））在SCID小鼠胫骨骨内注射模型中评估了药理性COX-2抑制的影响控制）。在治疗组中，每周3次以3 mg / Kg的剂量腹膜内使用CO- 2特异性抑制剂SC-58236，持续8周，直至处死。结果：COX-2的蛋白质印迹表明LAPC-9细胞表达高水平的COX-2，而PC-3细胞则不。与对照组相比，根据射线照相和组织形态计量学标准，SC-58236处理可显着减少LAPC-9注射后成骨细胞病变的大小。相反，在注射PC-3细胞后，在对照动物和SC-58236治疗的动物中均观察到较大的溶骨性病变。这项研究的结果表明，COX-2抑制作用可以减少LAPC-9产生的成骨性病变的大小，LAPC-9是一种表达高水平COX-2的人前列腺癌细胞系。该处理对PC-3细胞的溶骨活性没有影响。结论：这些发现提示人前列腺癌细胞诱导的成骨细胞转移的进程可能受到COX-2抑制剂的限制。

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