JNK信号通路受抑制的人白血病K562／ADR细胞对尼洛替尼敏感性

目的观察JNK信号通路受到抑制的人白血病K562／ADR细胞对尼洛替尼的敏感性。方法培养人白血病敏感细胞株K562和耐阿霉素细胞株K562／ADR，采用CCK_8法测算尼洛替尼对细胞的半抑制浓度（IC，。）及耐药指数。用4Ixg／mL的SP600125抑制K562／ADR细胞JNK信号通路后进行尼洛替尼处理，CCK一8法测算细胞尼洛替尼Ic。将K562／ADR细胞分为对照组、尼洛替尼组、联合组，对照组未处理，尼洛替尼组采用20Ixmol／L尼洛替尼处理，联合组先用4斗g／mLSP600125预处理2h，再用20Ixmol／L尼洛替尼处理，荧光定量PCR检测各组细胞内MDRl基因，Western...

Full description

Saved in:
Bibliographic Details
Published in山东医药 Vol. 57; no. 2; pp. 14 - 17
Main Author 严婧 何志旭 栾佐
Format Magazine Article
LanguageChinese
Published 贵州医科大学,贵阳,550004%北京海军总医院 2017
Subjects
JNK信号通路
SP600125
多药耐药1基因
尼洛替尼
白血病
leukemia
c-Jun N-terminal kinase
JNK信号通路
nilotinib
多药耐药1基因
multidrug resistance 1 gene
白血病
SP600125
尼洛替尼
Online AccessGet full text
ISSN1002-266X
DOI10.3969/j.issn.1002-266X.2017.02.004

Cover

More Information
Summary:目的观察JNK信号通路受到抑制的人白血病K562／ADR细胞对尼洛替尼的敏感性。方法培养人白血病敏感细胞株K562和耐阿霉素细胞株K562／ADR，采用CCK_8法测算尼洛替尼对细胞的半抑制浓度（IC，。）及耐药指数。用4Ixg／mL的SP600125抑制K562／ADR细胞JNK信号通路后进行尼洛替尼处理，CCK一8法测算细胞尼洛替尼Ic。将K562／ADR细胞分为对照组、尼洛替尼组、联合组，对照组未处理，尼洛替尼组采用20Ixmol／L尼洛替尼处理，联合组先用4斗g／mLSP600125预处理2h，再用20Ixmol／L尼洛替尼处理，荧光定量PCR检测各组细胞内MDRl基因，Westernblot法检测各组细胞内P．糖蛋白（P—gP）。结果K562／ADR细胞对尼洛替尼的耐药指数为K562细胞的19．58倍。抑制JNK信号通路后，尼洛替尼对K562／ADR细胞的IC，。由（12．53±0．11）Ixmol／L下降到（6．77±0．24）Ixmol／L（P〈0．05）。对照组、尼洛替尼组、联合组K562／ADR细胞MDRlmRNA相对表达量分别为0．9678-I-0．0062、0．5136±0．0124、0．2671±0．0087，P—gP相对表达量分别为1．0074-t-O．0041、0．5961±0．0136、0．3637±0．0069，两两组问比较，尸均〈0．05。结论JNK信号通路受抑制的人白血病K562／ADR细胞对尼洛替尼敏感性增加，这与抑制JNK信号通路可降低K562／ADR细胞中MDRl基因的表达有关。
Bibliography:37-1156/R
YAN Jing , HE Zhixu, LUAN Zuo （1 Guizhou Medical University, Guiyang 550004, China）
leukemia; multidrug resistance 1 gene; c-Jun N-terminal kinase; SP600125; nilotinib
Objective To observe the influence of inhibiting JNK signaling pathway on the sensitivity of K562/ADR cells to nilotinib. Methods The inhibitory concentration （ICs0） and resistance index of K562 cells and K562/ADR cells to nilotinib was measured by CCK-8 assay. K562/ADR cells were exposed to nilotinib after JNK signaling pathway was in- hibited by 4 Ixg/mL SP600125. CCK-8 assay was used to detect the IC50. K562/ADR cells were divided into the control group, nilotinib group and the combination group. The control group was not treated, nilotinib group was treated with 20 I~mol/L nilotinib, and the combination group was first treated with 4 p,g/mL SP600125 for 2 h, and then treated with 20 txmol/L nilotinib. The MDR1 gene was detected by real-time PCR. The P-glyeoprotein （P-g＇p） was detected by Western blotting. Results The resistance index
ISSN:1002-266X
DOI:10.3969/j.issn.1002-266X.2017.02.004