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硼替佐米对伊马替尼耐药细胞株K562/G01增殖抑制和诱导凋亡作用的 被引量:2

Growth inhibition and apoptosis induction to imatinib-resistant cell line K562/G01 by Bortezomib
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摘要 目的 探讨蛋白酶体抑制剂硼替佐米(BOR)对慢性粒细胞白血病(CML)伊马替尼耐药细胞株K562/C01的增殖抑制和诱导凋亡作用.方法 采用MTT法观察细胞的生长抑制效应;流式细胞术(FCM)榆测细胞周期与凋亡.结果 K562/C01细胞埘伊马替尼不敏感,伊马替尼对K562/C01和K562细胞的IC50分别是(20.09±1.38)、(0.54±0.13)μmol/L;BOR对K562/C01细胞具有增殖抑制作用,并于48h时作用效果达高峰,IC50(23.10±2.71)nmol/L,随着BOR浓度和作用时间的增加,FCM检测可见G2/M期细胞周期阻滞及明显的凋亡峰.结论 BOR对CML伊马替尼耐药细胞株具有增殖抑制和诱导凋亡的作用,其机制可能与细胞周期G2/M期的阻滞有关. Objective To explore the effect of proteasome inhibitor bortezomib (BOR) on proliferation inhibition and apoptosis in imatinib-resistant chronic myeloid leukemia cell line K562/G01. Methods MTT assay was used to observe the effect of growth inhibitory of cells; flow cytometry was used to detect cell cycle and apoptosis. Results K562/G01 cells was not sensitive to imatinib,1C50 values of imatinib to K562 and K562/G01 cells was (20.09±1.38) and (0.54±0.13) μmol/L,respectively; BOR could inhibit proliferation in K562/G01 cell,peaked at 48 h,and IC50 value of BOR to K562/G01 was (23.10±2.71) nmol/L. G2/M phase cell cycle arrest and significant apoptosis peak could be seen by flow cytometry with increased in the concentration and action time of BOR. Conclusion BOR can inhibit proliferation and induce apoptosis in imatinib-resistant K562/G01 cell,the mechanism may be related to cell cycle G2/M phase arrest.
出处 《白血病.淋巴瘤》 CAS 2010年第6期357-359,共3页 Journal of Leukemia & Lymphoma
关键词 白血病 髓样 慢性 肿瘤 实验性 硼替佐米 伊马替尼 K562/G01细胞 抗药性 肿瘤 Leukemia,myeloid,chronic Neoplasms,experimental Bortezomib Imatinib K562/G01 cell Drug resistance,neoplasms
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  • 1Cohen MH,Johnson JR,Pazdur RUS.Food and drug administration drug approval summary:conversion of imatinib mesylate (STI571;Gleevec) tablets from accelerated approval to full approval.Clin Cancer Res,2005,11:12-19.
  • 2Druker BJ,Guilhot F,0' Brien SG,et al.Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia.N Engl J Med,2006,355:2408-2417.
  • 3Gorre ME,Mohammed M,Ellwood K,et al.Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification.Science,2001,293:876-880.
  • 4Azam M,Latek RR,Daley GQ.Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL Cell,2003,112:831-843.
  • 5Quintds-Cardama A,Kantarjian HM,Cortes JE.Mechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia.Cancer Control,2009,16:122-131.
  • 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.
  • 7Katodritou E,Verrou E,Gastari V,et al.Response of primary plasma cell leukemia to the combination of bortezomib and dexamethasone:Do specific cytogenetic and immunophenotypic characteristics influence treatment outcome? Leuk Res,2008,32:1153-1156.
  • 8Baiz D,Pozzato G,Dapas B,et al.Bortezomib arrests the proliferation of hepatocellular carcinoma cells HepG2 and JHH6 by differentially affecting E2F1,p21 and p27 levels.Biochimie,2009,91:373-382.
  • 9Milano A,Iaffaioli RV,Caponigro F.The proteasome:a worthwhile target for the treatment of solid tumours? Eur J Cancer,2007,43:1125-1133.
  • 10Kelley TW,Alkan S,Srkalovic G,et al.Treatment of human chronic lymphocytic leukemia cells with the proteasome inhibitor bortezomib promotes apoptosis.Leuk Res,2004,28:845-850.

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