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蛋白酶体抑制剂联合亚砷酸对NB4细胞survivin基因表达的影响 被引量:1

Effect of proteasome inhibitor and As_2O_3 on expression of survivin mRNA in NB4 cells
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摘要 目的研究蛋白酶体抑制剂硼替佐米(bortezomib)单药应用及其联合亚砷酸(As2O3)对急性早幼粒细胞白血病(APL)细胞株NB4中survivin mRNA表达的影响。方法将受试对象分为9组:未加药空白对照组(D组);As2O3组,0.5μmol/L(A1组)和1μmol/L(A2组);bortezomib组,5nmol/L(B1组)和10nmol/L(B2组);联合组,0.5μmol/LAs2O3+5nmol/Lbortezomib(C1组),0.5μmol/LAs2O3+10nmol/Lbortezomib(C2组),1μmol/LAs2O3+5nmol/Lbortezomib(C3组),1μmol/LAs2O3+10nmol/Lbortezomib(C4组)。作用时间分为三个水平:24h,48h和72h。应用逆转录聚合酶链反应(RT-PCR)法检测药物作用前后抑凋亡基因survivinmRNA的表达水平。结果bortezomib和As2O3单药组中survivinmRNA的表达水平下降,且存在剂量与时间依赖性,联合组survivin mRNA的表达水平亦下降,且比单药组下降更明显。结论bortezomib与As2O3可通过抑制NB4细胞株survivin mRNA的表达诱导细胞发生凋亡,两药联合具有协同效应。 Objective To study the effect of bortezomib alone or combination of bortezomib and As2O3 on the expression of survivin mRNA in NB4 cells.Methods The subjects were divided into nine groups:control group(D group);As2O3 groups:0.5 μmol/L(A1 group)and 1 μmol/L(A2 group);bortezomib groups:5 nmol/L(B1 group)and 10 nmol/L(B2 group);combination groups:0.5 μmol/L As2O3+5 nmol/L bortezomib(C1 group),0.5 μmol/L As2O3+10 nmol/L bortezomib(C2 group),1 μmol/L As2O3+5 nmol/L bortezomib(C3 group),1 μmol/L As2O3+10 nmol/L bortezomib(C4 group).The drug interference lasted for 24 h,48 h and 72 h,respectively.The expression of survivin mRNA was determined by reverse transcription polymerase chain reaction(RT-PCR).Results The expression of survivin mRNA decreased in NB4 cells treated with bortezomib or As2O3 alone in a dose and time dependent manner,higher than that treated with combination of bortezomib and As2O3.Conclusion Bortezomib and As2O3 could induce apoptosis by inhibiting the expression of survivin mRNA in NB4 cells.Combination of bortezomib and As2O3 could have a synergistic effect.
出处 《山西医科大学学报》 CAS 2008年第3期218-221,共4页 Journal of Shanxi Medical University
关键词 蛋白酶体抑制剂 BORTEZOMIB AS2O3 NB4 survivin mRNA 凋亡 proteasome inhibitor bortezomib As2O3 NB4 survivin mRNA apoptosis
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参考文献10

  • 1Hideshima T, Mitsiades C, Akiyama M, et al. Molecular mechanisms mediating antimyelorna activity of proteasome inhibitor Ps341 [J ]. Blood, 2003,101 (4) : 1530 - 1534.
  • 2扶云碧,孙启鑫,孟凡义,谢军,周光飚.蛋白酶体抑制剂硼替佐米诱导髓系白血病细胞株 HL60凋亡的机制研究[J].中华医学杂志,2006,86(34):2413-2416. 被引量:14
  • 3Horton TM, Oannavarapu A, Blaney SM, et al. Bortezomib interactions with chemotherapy agents in acute leukemia in vitro [J ]. Cancer Chemother Pharmacol, 2006,58 ( 1 ) : 13 - 23.
  • 4Daj Y, Rahrnanj M, Pei XY, et al. Bortezornib and flavopiridol interact synergistically to induce apoptosis in chronic myeloid leukemia cells resistant to irnatinib mesylate through both Bcr/ Abl-dependent and - independent mechanisms [ J ]. Blood, 2004, 104(2) :509 - 518.
  • 5Ambrosini G, Adida C, Altieri DC. A novel anti-apoptosis gene, survivin, expressed in cancer and lymphorna [ J ]. Nature Med, 1997,3(8) :917 - 921.
  • 6Olie RA, Simoes-Wust AP, Baumann B, et al. A novel antisense oligonucleotide targeting survivin expression induces apoptosis and sensitizes lung cancer cells to chemotherapy[J ]. Cancer Res, 2000,60 ( 11 ) : 2805 - 2809.
  • 7Tamm I, Wang Y, Sausville E, et al. IAP-family protein survivin inhibits caspase activity and apoptosis induced by Fas ( CD95 ), Bax, caspase and anticancer drugs [J ]. Cancer Res, 1998, 58 (23):5315-5319.
  • 8Natarbartolo M, Cervello M, Dusonchet L, et al. Resistance to diverse apoptotic triggers in multidrug resistant HL-60 cells and its possible factors IAP (inhibitory of apoptosis proteins)[ J ]. Cancer Lett, 2002,180 : 91 - 101.
  • 9Mori A,Wada H,Nishimara Y, et al. Expression of antiapoptosis gene survivin in human leukemia [ J ]. Int J Hematol, 2002,75 : 161 - 165.
  • 10张卫国,谢国建,王启斌,王小虎,吴清明,王强,童强,李胜保.泛素-蛋白酶体抑制剂MG-132对食管癌细胞凋亡和生存素表达的影响[J].中国药房,2005,16(14):1055-1057. 被引量:4

二级参考文献27

  • 1江千里,孟凡义.肿瘤治疗新靶点:蛋白酶体抑制剂的基础和临床应用[J].中华医学杂志,2005,85(29):2085-2088. 被引量:3
  • 2Li M,Chen D,Shiloh A,et al .Deubiquitination of p53 by HAUSP is an important pathway for p53 stabilization[ J ]. Nature, 2002,416: 648.
  • 3He Q,Huang Y,Sheikh MS. Proteasomeinhibitor MG132 upregulates death receptor 5 and cooperates with Apo2-L/TRAIL to induce apoptosis in Bax-proficient and -deficient cells[J ]. Oncogene, 2004,23(14) :2 554.
  • 4Dai Y,Rahmani M,Pei XY,et al.Bortezomib and avopiridol interact synergistically to induce apoptosis in chronic myeloid leukemia cells resistant to imatinib mesylate through both Bcr/Abldependent and -independent mechanisms.Blood,2004,104:509-518.
  • 5Richardson PG,Hideshima T,Mitsiades C,et al.Proteasome inhibition in hematologic malignancies.Ann Med,2004,36:304-314.
  • 6O'Connor OA,Wright J,Moskowitz C,et al.Phase Ⅱ clinical experience with the novel proteasome inhibitor Bortezomib in patients with indolent non-Hodgkin's lymphoma and mantle cell lymphoma.J Clin Oncol,2005,23:676-684.
  • 7An WG,Hwang SG,Trepel JB,et al.Protease inhibitorinduced apoptosis:accumulation of wt p53,p21WAF1/CIP1,and induction of apoptosis are independent markers of proteasome inhibition.Leukemia,2000,14:1276-1283.
  • 8Zhang GS,Tu CQ,Zhang GY,et al.Indomethacin induces apoptosis and inhibits proliferation in chronic myelogenous leukemia cells.Leukemia Res,2000,24:385-392.
  • 9Adams J,Palombella V J,Sausville EA,et al.Proteasome inhibitors:a novel class of potent and effective antitumor agents.Cancer Res,1999,59:2615-2622.
  • 10Teicher BA,Ara G,Herbst R,et al.The proteasome inhibitor PS 341 in cancer therapy.Clin Cancer Res,1999,5:2638-2645.

共引文献16

同被引文献14

  • 1孙启鑫,孟凡义,扶云碧,李利.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[J].中国实验血液学杂志,2007,15(2):233-236. 被引量:15
  • 2Jiang CC, Lucas K, Avery-Kiejda KA, et al. Up-regulation of Mcl-1 is critical for survival of human melanoma cells upon endoplasmic reticulum stress. Cancer Res, 2008 ; 68 ( 16 ) : 6708 - 6717.
  • 3Huang DC, Strasser A. BH3-Only proteins-essential initiators of apoptotic cell death. Ce11,2000 ; 103 ( 6 ) :839 - 842.
  • 4Seo YW, Shin JN, Ko KH, et al. The molecular mechanism of Noxa-induced mitochondrial dysfunction in p53-mediated cell death. J Biol Chem,2003 ;278(48) : 482922 -48299.
  • 5Kim JY, Ahn HJ, Ryu JH, et al. BH3-Only protein Noxa is a mediator of hypoxic cell death induced by hypoxia-inducible factor lalpha. J Exp Med, 2004;199(1) :113 -124.
  • 6Sun Y, Leaman DW. Involvement of Noxa in cellular apoptofic responses to interferon, double-stranded RNA, and virus infection. J Biol Chem, 2005; 280(16) :15561 -15568.
  • 7Hershko T, Ginsberg D. Up - regulation of Bcl-2 homology 3 ( BH3 ) - only proteins by E2F1 mediates apoptosis. J Biol Chem, 2004;279 (10) :8627 -34.
  • 8Oda E, Ohki R, Murasawa H, et al. Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis. Science, 2000 ;288 (5468) : 1053 - 1058.
  • 9Lee S J, Kim KM, Namkoong S, et al. Nitric oxide inhibition of homocysteine-induced human endothelial cell apoptosis by down- regulation of p53-dependent Noxa expression through the formation of S-nitrosohomocysteine. J Biol Chem, 2005 ; 280 ( 7 ) : 5781 - 5788.
  • 10Sasaki T, Sasahira T, Shimura H, et al. Effect of human noxa on irinotecan-induced apoptosis in human gastric carcinoma cell lines. Hepatogastroenterology, 2004 ;51 (57) :912 - 915.

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