期刊文献+

腺病毒介导的新基因HA117对Jurkat细胞多药耐药功能的影响 被引量:3

Multidrug resistant function of adenovirus vector mediated novel gene HA117 in Jurkat cells
下载PDF
导出
摘要 目的研究新基因HA117对急性淋巴细胞白血病细胞Jurkat耐药性的影响,探讨新基因HA117多药耐药(multidrug resistance,MDR)相关功能。方法以携带HA117基因的重组腺病毒Ad5-HA117感染Jurkat细胞得到高表达HA117基因的细胞Jurkat/HA117,以荧光显微镜和流式细胞术检测细胞感染效率,RT-PCR检测感染前后实验细胞HA117基因表达,MTT检测比较高表达HA117基因前后Jurkat细胞药物敏感性变化。结果新基因HA117可使Jurkat细胞对多种化疗药物耐药性增强,转染Ad5-HA117重组腺病毒的Jurkat细胞对VCR、ADM、Vp-16、DNR、MMC、CTX药物的药物耐受性均比未转染的Jurkat细胞增高,增高3~7倍(P<0.05,P<0.01),转染空载体组耐药性跟未转染的Jurkat细胞相比无显著差异(P>0.05)。结论新基因HA117可使Jurkat细胞的耐药功能增加,证实新基因HA117具有多药耐药功能。 Objective To investigate the multidrug resistant function of the novel gene HA117 in human acute lymphoblastic leukemia cell line Jurkat. Methods The recombinant adenovirus Ad5-HA117 carrying HA117 gene was transfected into Jurkat cells for the harvest of Jurkat/HA117 cells highly expressing HA117 gene. The efficiency of cell infection was detected by fluorescent microscopy and cytometry. HA117 gene expressions in Jurkat cells before and after infection were detected by RT-PCR. Multidrug resistance function of the new gene HA117 was detected by multidrug resistance test. Results Jurkat/HAll7 cells expressed HA117 gene efficiently after infection with Ad5-HA117. The drug-resistance to DNR, ADM, CTX, VCR, MMC and VP-16 of Jurkat/HA117 cells enhanced as high as 3 -7 folds (P 〈0.05) than that to Jurkat cells. Conclusion The novel gene HA117 could enhance the multi-drug resistance of Jurkat cells, suggesting that HA117 gene might have multidrug resistant function.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2009年第16期1556-1558,共3页 Journal of Third Military Medical University
基金 国家自然科学基金(30471985)~~
关键词 新基因HA117 多药耐药 JURKAT细胞 novel gene HA117 multidrug resistance Jurkat cells
  • 相关文献

参考文献3

二级参考文献29

共引文献15

同被引文献43

  • 1蔺涛.肿瘤多药耐药的研究进展[J].海南医学,2006,17(12):140-142. 被引量:4
  • 2Beck R, Verrax J, Gonze T, et al. Hsp90 cleavage by an oxidative stress leads to its client proteins degradation and cancer cell death [ J ]. Biochem Pharmacol, 2009, 77 (3) : 375 - 383.
  • 3Chan C T, Paulmurugan R, Gheysens O S, et al. Molecular imaging of the efficacy of heat shock protein 90 inhibitors in living subjects [ J ]. Cancer Res, 2008, 68( 1 ) : 216 -226.
  • 4Chatteljee M, Jain S, Stuhmer T, et al. STAT3 and MAPK signaling maintain overexpression of heat shock proteins 90alpha and beta in multiple myeloma cells, which critically contribute to tumor-cell survival [J]. Blood, 2007, 109(2) : 720 -728.
  • 5Kurokawa M, Zhao C, Reya T, et al. Inhibition of apoptosome formation by suppression of Hsp90beta phosphorylation in tyrosine kinase-induced leukemias [J]. Mol Cell Biol, 2008, 28 ( 17 ) : 5494 - 5506.
  • 6Wu L X, Xu J H, Zhang K Z, et al. Disruption of the Bcr-Ab1/Hsp90 protein complex: a possible mechanism to inhibit Bcr-Abl-positive human leukemic blasts by novobiocin [ J ]. Leukemia, 2008, 22 ( 7 ) : 1402 - 1409.
  • 7Peng C, Brain J, Hu Y, et al. Inhibition of heat shock protein 90 prolongs survival of mice with BCR-ABL-T315I-induced leukemia and suppresses leukemic stem cells[J].Blood, 2007, 110(2) : 678 -685.
  • 8Lu Z, Jin Y, Qiu L, et al. Celastrol, a novel HSP90 inhibitor, depletes Bcr-Abl and induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T3151 mutation [ J ]. Cancer Lett, 2010, 290(2) : 182 -191.
  • 9Livak K J, Schmittgen T D. Analysis of relative gene expression data using real-time quantitative PCR and the 2 [-Delta Delta C (T)] Method[J]. Methods, 2001, 25(4) : 402 - 408.
  • 10Luo Q, Kang Q, Song w x, et al. Selection and validation of optimal siRNA target sites for RNAi-mediated gene silencing [J].Gene, 2007, 395 (1/2) : 160 - 169.

引证文献3

二级引证文献4

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