卡介苗诱导的巨噬细胞的二次刺激诱导膀胱癌细胞产生一氧化氮非依赖性细胞死亡。
Secondary stimulation from Bacillus Calmette-Guérin induced macrophages induce nitric oxide independent cell-death in bladder cancer cells.
机构信息
Department of Urology, Karolinska University Hospital, Stockholm, Sweden; Urology Laboratory, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Department of Urology, Karolinska University Hospital, Stockholm, Sweden; Urology Laboratory, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Laboratory Medicine, Division of Clinical Chemistry, Karolinska Institutet and Karolinska University Hospital Huddinge, Stockholm, Sweden; Stockholm University, Department of Genetics, Microbiology and Toxicology, Stockholm, Sweden.
出版信息
Cancer Lett. 2014 Jun 28;348(1-2):119-25. doi: 10.1016/j.canlet.2014.03.014. Epub 2014 Mar 18.
The anti-tumour mechanisms following Bacillus Calmette-Guérin (BCG) treatment of bladder-cancer remain largely unknown. Previous studies have shown involvement of nitric-oxide (NO) formation in the BCG-mediated effect. We analyzed the effects of macrophage secreted factors (MSFs) from BCG-stimulated RAW264.7 cells on the bladder-cancer cell line MBT2. Direct treatment with BCG did not induce NO in MBT2-cells whereas supernatant from BCG-stimulated macrophages increased NOS2 mRNA and protein expression, NO concentrations and cell-death. Blocking NO-synthesis with the NOS-inhibitor L-NAME did not affect levels of cell-death suggesting cytotoxic pathways involving other signalling molecules than NO. Several such candidate genes were identified in a microarray.
BCG 治疗膀胱癌的抗肿瘤机制在很大程度上尚不清楚。先前的研究表明，一氧化氮（NO）的形成参与了 BCG 介导的作用。我们分析了来自 BCG 刺激的 RAW264.7 细胞的巨噬细胞分泌因子（MSFs）对膀胱癌细胞系 MBT2 的影响。BCG 直接处理不会诱导 MBT2 细胞中的 NO，而来自 BCG 刺激的巨噬细胞的上清液则增加了 NOS2 mRNA 和蛋白表达、NO 浓度和细胞死亡。用 NOS 抑制剂 L-NAME 阻断 NO 合成不会影响细胞死亡水平，这表明细胞毒性途径涉及比 NO 更复杂的信号分子。在基因芯片中鉴定了几个这样的候选基因。
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