中文摘要：

目的探讨前动力蛋白（prokineticin-1，Prok-1）对神经母细胞瘤细胞QDDQ-NM细胞血管生成的影响。方法应用Prok-1蛋白受体基因PKRl小分子干扰RNA（small interferingRNA，siRNA）转染人神经母细胞瘤QDDQNM细胞，分别用Prok-1、AKT蛋白激酶抑制剂LY294002处理后，采用Westernblot检测AKT蛋白磷酸化水平，采用酶联免疫吸附实验（ELISA）检测细胞培养上清内血管内皮生长因子（VEGF）的含量。结果Prok-1可激活ATK信号通路，磷酸化AKT蛋白水平升高；同时上调QDDQ-NM细胞VEGF的表达。在Prok-1蛋白激酶抑制剂处理浓度分别为0和100ng／ml时，培养细胞上清VEGF浓度分别为（212±23）pg／ml和（416±43）pg／ml，两者差异有统计学意义（P〈0．01）。而AKT蛋白激酶抑制剂LY~294002可抑制Prok-1上调VEGF的表达。结论Prok1可能通过AKT信号传导途径上调神经母细胞瘤VEGF的表达，促进肿瘤血管形成，进而促进神经母细胞瘤的增殖和转移。

英文摘要：

Objective To investigate the influence of prokineticin-I （Prok-1）on VEGF expression in neuroblastoma cell line （QDDQ-NM）. Methods Prokineticin-1 receptor gene（PKR1 ）small interfering RNA was transfected into neuroblastoma QDDQ-NM cells. The Prok-1 and AKT protein ki- nase inhibitor LY294002 was respectively administered to have effect on AKT signaling pathway in cells. Western blot was conducted to detect the level of AKT-p, and the production of VEGF in supernatant was detected using ELISA assay. Results Prok-1 could activate the ATK signaling pathway and increased AKT-p level; meanwhile, the production of VEGF in QDDQ-NM cells was improved. Compared with control, 100 ng/ml concentration of prokineticin-1 induced an increased expression of VEGF protein in post co-culture 24 h （416± 43 pg/ml versus 212 ±23 pg/ml,P〈0. 01 ）. On the contrary, LY-294002 inhibited Prok-1 induced up-regulation of VEGF. Conclusions Prokineticin-1 increa ses the expression of VEGF by activating the AKT signaling pathway, through which the angiogenesis in tumor tissue is promoted and the following tumor cells proliferation and metastasis.