期刊文献+

硼替佐米单用或联合三尖杉酯碱体外诱导HL-60细胞凋亡实验研究 被引量:15

Induction of Apoptosis in HL-60 Cells by Bortezomib alone or in Combination with Harringtonine In Vitro
下载PDF
导出
摘要 本研究探讨硼替佐米(bortezomib,Bor)单用或联合三尖杉酯碱(harringtonine,HT)对HL-60细胞凋亡的影响。以不同浓度Bor、HT处理HL-60细胞12-48小时,采用MTT比色法检测细胞增殖活性,以DNA凝胶电泳、荧光显微镜检、流式细胞术检测细胞凋亡。结果表明:10-50nmol/LBor可有效抑制HL-60细胞增殖,并诱导其凋亡。其中10nmol/L剂量处理12小时即有细胞凋亡发生,延长作用时间或增加药物剂量可使细胞凋亡率明显增加。30nmol/LHT与10nmol/LBor联合应用时,可见HL-60细胞凋亡率比两种药物单独使用时显著增加。结论:Bor对HL-60细胞具有时间和剂量依赖性的细胞凋亡诱导效应,与HT联合应用有明显的协同作用。 The aim of this study was to investigate the effect of bortezomib alone and in combination with harringtonine on apoptosis of HL-60 cells. ILL-60 cells were treated with bortezomib, harringtonine in different concentrations for 12 -48 hours. Cell proliferation was analyzed by MTT assay; the apoptosis of HL-60 cells was observed by DNA gel electrophoresis, fluorescence microscopy and flow cytometry. The results showed that 10 -50 nmol/L bortezomib could effectively inhibit HL-60 cell proliferation, and induced its apoptosis. After treating for 12 hours, 10 nmol/L bortezomib could trigger cells apoptosis. With time prolongation or dose increase, HL-60 cell apoptotic rate significantly increased. Furthermore, co-administration of bortezomib (10 nmol/L) with harringtonine (30 nmol/L) resulted in a higher cell apoptotic rate when compared with that induced by those agents used alone. It is concluded that the bortezomib can induce HL-60 cells apoptosis in a time-and-dose-dependent manner and synergistic effectiveness can be found when bortezomib combined with harringtonine.
出处 《中国实验血液学杂志》 CAS CSCD 2007年第2期233-236,共4页 Journal of Experimental Hematology
基金 广东省科技攻关项目(B30202)
关键词 硼替佐米 三尖杉酯碱 凋亡 bortezomib harringtonine apoptosis
  • 相关文献

参考文献11

  • 1Boccadoro M,Morgan G,Cavenagh J.Preclinical evaluation of the proteasome inhibitor bortezomib in cancer.Cancer Cell Int,2005;5:18-27 被引量:1
  • 2D.L.斯佩克特著(黄培堂等译).细胞实验指南.北京:科学出版社.2001:108-109 被引量:1
  • 3兰雨,张学敏,胡美茹,杨怡,杨平地,沈倍奋.阻断泛素-蛋白酶体通路诱导白血病细胞凋亡及机制探讨[J].中国实验血液学杂志,2001,9(2):105-109. 被引量:5
  • 4Voorhees PM,Dees EC,ONeil B,et al.The proteasome as a target for cancer therapy.Clin Cancer Res,2003; 9:6316-6325 被引量:1
  • 5Gatto S,Scappini B,Pham L,et al.The proteasome inhibitor PS341 inhibits growth and induces apoptosis in Bcr/Abl-positive cell lines sensitive and resistant to imatinib mesylate.Haematologica,2003; 88:853-863 被引量:1
  • 6Horton TM,Gannavarapu A,Blaney SM,et al.Bortezomib interactions with chemotherapy agents in acute leukemia in vitro.Cancer Chemother Pharmacol,2006; 58:13-23 被引量:1
  • 7Dai Y,Rahmani M,Pei XY,et al.Bortezomib and flavopiridol interact synergistically to induce apoptosis in chronic myeloid leukemia cells resistant to imatinib mesylate through both Bcr/Abl-dependent and -independent mechanisms.Blood,2004; 104:509-518 被引量:1
  • 8Dai Y,Rahmani M,Grant S,et al.Proteasome inhibitors potentiate leukemic cell apoptosis induced by the cyclin-dependent kinase inhibitor flavopiridol through a SAPK/JNK-and NF-kappaB-dependent process.Oncogene,2003; 22:7108-7122 被引量:1
  • 9Smolewski P,Duechler M,Linke A,et al.Additive cytotoxic effect of bortezomib in combination with anti-CD20 or anti-CD52 monoclonal antibodies on chronic lymphocytic leukemia cells.Leuk Res,2006; 30:1521-1529 被引量:1
  • 10Cortes J,Thomas D,Koller C,et al.Phase I study of bortezomib in refractory or relapsed acute leukemias.Clin Cancer Res,2004; 10:3371-3376 被引量:1

二级参考文献10

  • 1Adams J, Palombella VJ, Sausville EA, et al. Proteasome inhibitors: a novel class of potent and effective antitumor agents. Cancer Res, 1999; 59:2615 - 2622 被引量:1
  • 2Orlowski RZ. The role of the ubiquitin-proteasome pathwayin apoptosis. Cell Death Differ, 1999; 6:303- 313 被引量:1
  • 3Drexler HC. Activation of the cell death program by inhibition of proteasome function. Proc Natl Acad Sci USA,1997; 94:855 - 860 被引量:1
  • 4Zhang XM, Lin H, Chen C, et al. Inhibition of ubiquitin-proteasome pathway activates a caspase-3-like protease andinduces Bcl-2 cleavage in human M-07e leukaemic cells.Biochem J, 1999; 340(Pt 1): 127- 133 被引量:1
  • 5Chen C, Lin H, Karanes C, et al. Human THP-1 mono-cytic leukemic cells induced to undergo monocytic differenti-ation by bryostatin 1 are refractory to proteasome inhibitor-induced apoptosis. Cancer Res, 2000; 60:4377- 4385 被引量:1
  • 6Izban KF, Wrone-Smith T, Hsi ED, et al. Characteriza-tion of the interleukin-1beta-converting enzyme/ced-3-familyprotease, caspase-3/CPP32, in Hodgkin′s disease: lack ofcaspase-3 expression in nodular lymphocyte predominanceHodgkin′s disease. Am J Pathol, 1999; 154:1439-1447 被引量:1
  • 7Cheng EH, Kirsch DG, Clem RJ, et al. Conversion ofBcl-2 to a Bax-like death effector by caspases. Science,1997; 278:1966 - 1968 被引量:1
  • 8Thomberry NA, Lazebnik Y. Caspases: enemies within.Science, 1998; 281:1312 - 1316 被引量:1
  • 9.SwantonE,SavoryP,CosulichS,etal.Bcl-2regulatesacaspase-3/caspase-2apoptoticcascadeincytosolicextracts.Oncogene,1999;18:1781-1787 被引量:1
  • 10胡美茹,兰雨,张学敏,沈倍奋.Caspase与Bcl-2在凋亡发生和调控中的相互作用机制[J].军事医学科学院院刊,2000,24(2):126-129. 被引量:19

共引文献4

同被引文献113

引证文献15

二级引证文献20

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部