Establishment of new prostate cancer metastatic model with androgen independent growth and identification of new mechanism of androgen-independency

我们从TRAP肿瘤中建立了雄激素非依赖性前列腺癌细胞系，命名为PCai1，并报道了利用PCai1细胞原位转移模型和尾静脉注射模型。采用RT-PCR和Western blot检测pca1 GST-P的表达。此外，我们利用GST-P-siRNA研究了PCai1细胞生长与活性氧（Reactive Oxygen Species， ROS）的关系。在Charcoal stripping - fbs培养基中，PCai1细胞GST-P mRNA和蛋白表达水平均高于正常培养基。siRNA敲除GST-P后，体外细胞增殖率明显降低。相反，DCFH实验显示GST-P-siRNA处理可诱导ROS。静脉注射后骨髓转移的肿瘤表达高水平的GST-P，而原位植入的肺和淋巴结转移灶未表达GST-P。GST-P可能通过抑制ROS在前列腺癌的生长和转移中发挥重要作用。

We established androgen-independent prostate cancer cell line from TRAP tumor, and named PCai1, and previously reported the orthotopic metastatic models, and tail vein injection model using PCai1 cells. We investigate the GST-P expression of PCai1 by RT-PCR and Western blot. In addition, using GST-P-siRNA, we investigated the relationship between the cell growth and Reactive Oxygen Species(ROS) in PCai1.PCai1 cells had higher GST-P expression in mRNA and protein levels in Charcoal Stripped-FBS medium than in normal medium. GST-P knocked down by siRNA resulted in significant decrease of the proliferation rate in vitro. On the contrary, DCFH assay revealed that ROS was induced by GST-P-siRNA treat. Tumors metastasized in the bone marrow after intravenous injection expressed high levels of GST-P, while metastatic lesions in the lung and lymph nodes failed to express GST-P as seen in the case of the orthotopic implantation. GST-P might have the important roles in the prostate cancer growth and metastasis by the restriction of ROS.