Imatinib mesylate induces apoptosis of K562 cell by down-regulating miR-139

被引:0
|
作者
Wang, Linhui [1 ]
Guo, Pengxiang [1 ]
机构
[1] Peoples Hosp Guizhou Prov, Dept Hematol, 83 Zhongshan East Rd, Guiyang 550001, Guizhou, Peoples R China
关键词
Imatinib mesylate; microRNA-139; K562; cells; leukemia; cell apoptosis; CHRONIC MYELOID-LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; RESISTANCE; INHIBITOR; PATHWAY; KINASE; COMBINATION; ACTIVATION; EXPRESSION; SURVIVAL;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Leukemia has severely endangered people healthy. Imatinib mesylate is a newly-developed targeting drug for treating leukemia. This study aimed to investigate the molecular mechanism of imatinib mesylate on regulating K562 cell apoptosis via mediating micro RNA-139 (miR-139) expression. K562 cells were treated with imatinib mesylate and were examined for their growth, proliferation and apoptosis by flow cytometry. MiR-139 expression level was determined by RT-PCR. We also synthesized miR-139 expressing vectors and transfected them into K562 cells, followed by imatinib mesylate treatment and cell viability and apoptotic assays. The inhibition of K562 cell growth and proliferation occurred after imatinib mesylate treatment, accompanied with cell apoptosis. In leukemia patient sample, the expression level of miR-139 was significantly higher than normal people. K562 cell over-expressing miR-139 had depressed level of imatinib mesylate-induced cell apoptosis. Imatinib mesylate induces the apoptosis of K562 cells via suppressing miR-139 expression.
引用
收藏
页码:7863 / 7869
页数:7
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