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Bay117802抑制羟基喜树碱诱导的人乳腺癌Bcap37细胞凋亡 被引量：3

Inhibition of NF-kappa B activation by Bay117082 attenuate apoptosis induced by HCPT in Breast cancer Bcap 37 cells
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摘要 目的:探讨IκB-α磷酸化抑制剂Bay117082特异性阻断NFκB信号转导途径对羟基喜树碱(HCPT)诱导Bcap37细胞凋亡的影响。方法:采用MTT法测定细胞的增殖活力;琼脂糖凝胶电泳观察细胞调亡;Western blot研究细胞调亡所涉及的蛋白表达;DIG-EMSA研究NFκB/DNA结合状况。结果:5μmol.L-1Bay117082可以抑制HCPT对IκB-α的磷酸化,阻断NFκB信号转导途径,阻滞HCPT诱导的细胞凋亡,同时也抑制HCPT诱导pro-Caspase3和Bcl-2的降解。结论:Bay117082对HCPT诱导的乳腺癌细胞凋亡有明显的抑制作用,其作用机制与NFκB信号转导途径有关,NFκB起促进凋亡的作用。 AIM： To investigate the role of Bay117082 in apoptosis induced by 10-Hydroxycamptothecin （HCPT） in human breast carcinoma cells. METHODS： The cell growth inhibiting was measured by MTT assay, agarose gel eletrophoresis were performed for cell apoptosis, Western Blotting were performed for protein expression. DIG-EMSA was conducted to determine the DNA-binding activation of NF kB. RESULTS： 5mmol· L^-1 Bay117082 had a remarkable inhibition on apoptosis induced by HCPF in breast cancer cells. NF kB was not activated after exposing to HCPT plus Bay117082. Pro-Caspase3 and Bcl-2 were not degraded either. CONCLUSION： Bay117082 may attenuate apoptosis induced by HCPT through inhibiting activation of NF kB in Bcap37 cell line.
作者 叶孟 林蕾 方勇 潘宏铭 吴金民
机构地区 宁波大学附属医院肿瘤科 浙江大学附属邵逸夫医院肿瘤中心
出处 《中国临床药理学与治疗学》 CAS CSCD 2005年第7期755-759,共5页 Chinese Journal of Clinical Pharmacology and Therapeutics
关键词 羟基喜树碱 乳腺癌 凋亡 Bay117802 核转录因子KB HCPT breast carcinoma cell apoptosis Bay117082 NFkB
分类号 R979.1 [医药卫生—药品]
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参考文献9

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同被引文献29

  • 1叶孟,林蕾,方勇,潘宏铭,吴金民.羟基喜树碱依赖Caspase3途径诱导人乳腺癌Bcap37细胞凋亡[J].中国临床药理学与治疗学,2005,10(8):881-884. 被引量：6
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中国临床药理学与治疗学
2005年 第7期

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