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作 者:钱敏[1,2] 王世宣[1] 王鸿雁[1] 卢运萍[1] 马丁[1] 刘荣华[1]
机构地区:[1]华中科技大学同济医学院附属同济医院肿瘤生物医学中心教育部肿瘤侵袭与转移重点实验室,武汉市430030 [2]南京军区南京总医院妇产科
出 处:《中国肿瘤临床》2012年第21期1608-1611,共4页Chinese Journal of Clinical Oncology
基 金:国家重点基础研究发展规划(973)项目(编号:2009CB521800)资助~~
摘 要:目的:探讨BAY11-7082对前列腺癌细胞NF-κB表达及其生物学行为的影响。方法:应用CCK-8方法、蛋白印迹、NF-κB激活-核转运检测,细胞增殖抑制实验和集落形成实验方法观察BAY11-7082作用下前列腺癌细胞NF-κB蛋白的表达,细胞生长等指标的变化。结果:BAY11-7082对前列腺癌细胞转移有明显的抑制作用。BAY11-7082处理的前列腺癌细胞内NF-κB蛋白表达降低,减弱NF-κB的激活,细胞增殖和形成集落的能力下降。结论:BAY11-7082可抑制前列腺癌细胞NF-κB的激活与表达,提示NF-κB可作为前列腺癌基因治疗的重要靶点之一。Objective: This study was designed to determine the effect of BAY 11-7082 on NF-~cB expression and tumor colony formation of prostate cancer cells. Methods: Cell cytotoxicity assay kit-8 was used to detect cell death and proliferation according to the protocol. Western blot and densitometry analysis were performed to compare the expression of NF-KB in the control group with that of BAY 11-7082, an NF-nB inhibitor that is used to treat prostate cancer cells. Immunofluorescent staining was also conducted to moni- tor NF-KB activation and translocation in the nucleus. The effects of BAY 11-7082 on colony formation were determined by counting the number of prostate cancer cell colonies. Results: The treatment of prostate cancer cell line PC-3 cells by BAY 11-7082 inhibited cell proliferation and formed few colonies. Similarly, NF-tcB protein level dramatically decreased. Its translocation in the nucleus and the activation in the PC-3 cells were disrupted because of the effects of BAY 11-7082. Conclusion: BAY 11-7082 can inhibit the aberrant activation of NF-κB in prostate cancer cells and reduce tumor metastasis. Therefore, BAY 11-7082 is a potential drug for the treatment of prostate cancer patients in clinical practice in the future.
关 键 词:前列腺癌 NF-ΚB BAY11-7082 转移
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