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Gambogic acid induces mitochondria-dependent apoptosis by modulation of Bcl-2 and Bax in mantle cell lymphoma JeKo-1 cells 被引量:18
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作者 Jingyan Xu Min Zhou +7 位作者 Jian Ouyang Jing Wang Qiguo Zhang Yong Xu Yueyi Xu Qian Zhang Xihui Xu Hui Zeng 《Chinese Journal of Cancer Research》 SCIE CAS CSCD 2013年第2期183-191,共9页
Objective: To study the mechanisms in gambogic acid (GA) -induced JeKo-1 human Mantle Cell Lymphoma cell apoptosis in vitro. Methods: The proliferation of GA-treated JeKo-1 cells was measured by CCK-8 assay and Ki... Objective: To study the mechanisms in gambogic acid (GA) -induced JeKo-1 human Mantle Cell Lymphoma cell apoptosis in vitro. Methods: The proliferation of GA-treated JeKo-1 cells was measured by CCK-8 assay and Ki-67 immunocytochemical detection. Apopt0sis, cell cycle and mitochondrial membrane potential were measured by flow cytometric analysis. Caspase-3, -8 and -9 were detected by colorimetric assay. Bcl-2 and Bax were analyzed by Western blotting. Results: GA inhibited cell growth in a time- and dose- dependent manner. GA induces apoptosis in JeKo- 1 cells but not in normal bone marrow cells, which was involved in reducing the membrane potential of mitochondria, activating caspases-3, -8 and -9 and decreasing the ratio of Bd-2 and Bax without cell cycle arresting. Conclusions: GA induced apoptosis in human MCL JeKo-1 cells by regulating Bcl-2/Bax and activating caspase-3, -8 and -9 via mitochondrial pathway without affecting cell cycle. 展开更多
关键词 Gambogic acid jeko-1 cells cell cycle arrest apoptosis membrane potential of mitochondria caspase-3 CASPASE-8 caspase-9 BAX BCL-2
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咪达唑仑对套细胞淋巴瘤细胞系JeKo-1的作用及机制研究 被引量:1
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作者 洪金全 吴珊瑚 +2 位作者 陈志远 庄伟煌 高宏志 《中国实验血液学杂志》 CAS CSCD 北大核心 2013年第6期1460-1463,共4页
本研究探讨咪达唑仑(midazolam)对套细胞淋巴瘤细胞系JeKo-1的作用及相关机制。采用CCK8法观察咪达唑仑对JeKo-1细胞增殖的影响;流式细胞术分析咪达唑仑对JeKo-1细胞凋亡的影响;Western blot法检测咪达唑仑对JeKo-1细胞BCL-2、细胞色素C... 本研究探讨咪达唑仑(midazolam)对套细胞淋巴瘤细胞系JeKo-1的作用及相关机制。采用CCK8法观察咪达唑仑对JeKo-1细胞增殖的影响;流式细胞术分析咪达唑仑对JeKo-1细胞凋亡的影响;Western blot法检测咪达唑仑对JeKo-1细胞BCL-2、细胞色素C(Cyto-C)、pro-caspase-9、pro-caspase-8、pro-caspase-3蛋白表达的影响。结果表明,咪达唑仑能明显抑制JeKo-1细胞增殖,48 h的半数抑制浓度(IC50)约为40μmol/L;不同浓度咪达唑仑处理48 h后JeKo-1细胞出现凋亡,呈现剂量依赖性;同时,JeKo-1细胞内BCL-2、pro-caspase-9、pro-caspase-3蛋白表达呈剂量依赖性降低,Cyto-C蛋白表达呈相应增加,而pro-caspase-8蛋白表达则未发生变化。结论:咪达唑仑可能通过下调JeKo-1细胞BCL-2的表达,触发线粒体凋亡途径,但不活化死亡受体途径,导致线粒体Cyto-C的释放,并引发caspase-9、caspase-3的活化,启动了caspase级联反应,最终导致了JeKo-1细胞的凋亡。 展开更多
关键词 咪达唑仑 套细胞淋巴瘤 jeko-1细胞系
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西达本胺对利妥昔单抗耐药B细胞淋巴瘤增殖的影响及作用机制
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作者 柯晴 罗瞾 岑洪 《中国癌症防治杂志》 CAS 2020年第5期543-548,共6页
目的探讨组蛋白去乙酰化酶(HDAC)抑制剂西达本胺在体外对利妥昔单抗耐药的B细胞淋巴瘤细胞增殖的影响及其可能的作用机制。方法采用不同浓度西达本胺、利妥昔单抗单药或联合作用于淋巴瘤Jeko-1和Jeko-1/R细胞,采用CCK-8法检测细胞增殖情... 目的探讨组蛋白去乙酰化酶(HDAC)抑制剂西达本胺在体外对利妥昔单抗耐药的B细胞淋巴瘤细胞增殖的影响及其可能的作用机制。方法采用不同浓度西达本胺、利妥昔单抗单药或联合作用于淋巴瘤Jeko-1和Jeko-1/R细胞,采用CCK-8法检测细胞增殖情况;RT-PCR检测CD20 mRNA表达水平;Western blot法检测组蛋白H3、H4的乙酰化水平。结果25μg/mL、50μg/mL、100μg/mL和200μg/mL利妥昔单抗在48 h可呈剂量依赖式抑制Jeko-1细胞增殖,组间差异有统计学意义(F=38.533,P<0.001),且细胞增殖抑制率均高于Jeko-1/R细胞(均P<0.001)。4μmol/L、8μmol/L和16μmol/L西达本胺在48 h呈剂量依赖式抑制Jeko-1和Jeko-1/R细胞增殖,组间差异有统计学意义(F=17.968,P=0.003;F=51.456,P<0.001),但不同浓度西达本胺作用Jeko-1和Jeko-1/R细胞的增殖抑制率差异均无统计学意义(均P>0.05)。西达本胺(8μmol/L)联合利妥昔单抗(100μg/mL)分别处理Jeko-1和Jeko-1/R细胞48 h,与单药西达本胺比较,联合处理后细胞增殖抑制率均增高(P<0.001)。西达本胺在48 h呈剂量依赖式上调Jeko-1/R细胞CD20 mRNA表达和组蛋白H3和H4乙酰化水平(P<0.001)。结论西达本胺可抑制耐药B细胞淋巴瘤Jeko-1/R细胞增殖,其作用机制可能与上调组蛋白H3、H4乙酰化水平及CD20 mRNA表达有关。 展开更多
关键词 B细胞淋巴瘤 jeko-1/R细胞 组蛋白去乙酰化酶抑制剂 西达本胺 利妥昔单抗 CD20
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