[1]许严伟)△,赵小利),王英),等.伊马替尼敏感及耐药K562细胞P糖蛋白、缺氧诱导因子和鞘氨醇激酶表达的比较*[J].郑州大学学报(医学版),2012,(02):153.
 XU Yanwei),ZHAO Xiaoli),WANG Ying),et al.Comparison of expressions of Pglycoprotein,HIF1α,and SPK between K562 and K562/Ima cells[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2012,(02):153.
点击复制

伊马替尼敏感及耐药K562细胞P糖蛋白、缺氧诱导因子和鞘氨醇激酶表达的比较*
分享到:

《郑州大学学报(医学版)》[ISSN:1671-6825/CN:41-1340/R]

卷:
期数:
2012年02期
页码:
153
栏目:
论著
出版日期:
2012-03-20

文章信息/Info

Title:
Comparison of expressions of Pglycoprotein,HIF1α,and SPK between K562 and K562/Ima cells
作者:
许严伟1)赵小利1)王英1)苗润宏1)张庆林2)杜钢军3)
1)洛阳市第三人民医院药剂科 洛阳 471002 2)北京军事医学科学院 北京 100850 3)河南大学药学院 开封 475001
Author(s):
XU Yanwei1)ZHAO Xiaoli1)WANG Ying1)MIAO Runhong1)ZHANG Qinglin2)DU Gangjun3)
1)Department of Pharmacy,Luoyang Third People’s Hospital, Luoyang 471002 2)Academy of Military Medical Sciences,Beijing 100850 3)Pharmaceutial College,Henan University, Kaifeng 475001
关键词:
伊马替尼K562P糖蛋白鞘氨醇激酶缺氧诱导因子1α
Keywords:
imatinibK562PglycoproteinSPKHIF1α
分类号:
R966
摘要:
目的:比较伊马替尼敏感及耐药K562(K562/Ima)细胞P糖蛋白、缺氧诱导因子1α和鞘氨醇激酶表达的差异。方法:取对数生长期的K562和K562/Ima细胞,采用不同质量浓度的伊马替尼分别处理48 h,应用MTT法计算耐药倍数;另取上述2种细胞,分别采用Western blot、RTPCR及同位素掺入等方法检测2种细胞中P糖蛋白、缺氧诱导因子1α和鞘氨醇激酶的表达。结果:相对于K562细胞,K562/Ima细胞的耐药倍数为24。在K562/Ima细胞中,P糖蛋白、缺氧诱导因子1α和鞘氨醇激酶的表达均高于K562细胞。结论:K562/Ima的耐药机制与P糖蛋白、缺氧诱导因子、鞘氨醇激酶等基因的表达上调有关。
Abstract:
Aim:To compare the expressions of Pglycoprotein(Pgp),HIF1α,and SPK between chronic myeloid leukemia cell line K562 and imatinibresistance K562(K562/Ima)cell line.Methods:K562 and K562/Ima cells were treated with different doses of imatinib for 48 h,and MTT was used to calculate the resistance fold.Western blot,RTPCR and TLC were used to detect the expressions of Pgp,HIF1α and SPK in K562 and K562/Ima cells,respectively.Results:The results revealed K562/Ima cells showed 24 fold resistance to imatinib compared with K562 cells.The expressions of Pgp,SPK and HIF1α were upregulated in K562/Ima cells.Conclusion:It is concluded that the resistance of K562/Ima cells is related to the high expressions of Pgp,SPK and HIF1α.

参考文献/References:

[1]GarciaManero G,Talpaz M, Kantarjian HM. Current therapy of chronic myelogenous leukemia[J]. Intern Med,2002,41(4):254
[2]Goldman JM. Chronic myeloid leukemia—still a few questions [J]. Exp Hematol,2004,32(1):2
[3]张琳,周健,蒋东霞. 伊马替尼对人CD34+来源树突状细胞体外分化和功能的影响[J]. 郑州大学学报:医学版,2006,41(4):742
[4]Olivera A, Kohama T, Tu Z,et al. Purification and characterization of rat kidney sphingosine kinase[J].J Biol Chem,1998,273(2D):12576
[5]Nava VE, Lacana E, Poulton S,et al. Functional characterization of human sphingosine kinase1[J].FEBS Lett, 2000, 473(1): 81
[6]Semenza GL. Targeting HIF1α for cancer therapy[J].Nat Rev Cancer,2003,3(10):721
[7]赵富周,杨鲲鹏,庞志刚,等.食管鳞状细胞癌组织中HIF1α、CCR7 和 VEGF C 蛋白的表达[J]. 郑州大学学报:医学版,2011,46(5):660
[8]Comerford KM, Wallace TJ, Karhausen J,et al. Hypoxia inducible factor1α dependent regulation of the multidrug resistance (MDR1 )gene [J].Cancer Res,2002,62(12):3387

相似文献/References:

[1]孙黎),程建贞),罗强),等.金莲花黄酮对K562、HeLa、Ec109、NCIH446细胞增殖的影响*[J].郑州大学学报(医学版),2009,(05):981.
 SUN Li),CHENG Jianzhen),LUO Qiang),et al.Effects of Trollius flavonoids on proliferation of K562,HeLa,Ec109, and NCIH446 tumor cells[J].JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES),2009,(02):981.

备注/Memo

备注/Memo:
*国家自然科学基金资助项目30472082 男,1981年3月生,硕士,药师,研究方向:肿瘤药理学,Email:xywvip118@163.com
更新日期/Last Update: 1900-01-01