Endothelial-monocyte-activating polypeptide II induces rat C6 glioma cell apoptosis via the mitochondrial pathway

被引：8
作者：
Liu, Li-bo [1 ,2 ]
Xie, Hui [1 ,2 ]
Xue, Yi-xue [1 ,2 ]
Liu, Yun-hui [3 ]
Li, Zhen [3 ]
Wang, Ping [1 ,2 ]
机构：
[1] China Med Univ, Coll Basic Med, Dept Neurobiol, Shenyang 110001, Liaoning Provin, Peoples R China
[2] China Med Univ, Inst Pathol & Pathophysiol, Shenyang 110001, Peoples R China
[3] China Med Univ, Shengjing Hosp, Dept Neurosurg, Shenyang 110001, Peoples R China
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2015年 / 457卷 / 04期
关键词：
EMAP II; Apoptosis; Glioma; Reactive oxygen species; Bax; Bcl-2; BLOOD-TUMOR BARRIER; PERMEABILITY;
D O I：
10.1016/j.bbrc.2015.01.030
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
The present study was performed to examine whether Endothelial-monocyte-activating polypeptide II (EMAP II) could inhibit glioma growth by inducing rat brain glioma C6 cells apoptosis. The results revealed that the EMAP II decreased cell viability of rat C6 glioma cells in a time-dependent manner. Apoptotic proportion was increased gradually after EMAP II. EMAP II induced the decrease in mitochondrial membrane potential and the release of cytochrome c into the cytosol, followed by activation of caspase-9 and caspase-3. Meanwhile, EMAP II-induced apoptosis was accompanied by an increase of reactive oxygen species (ROS). The significant up-regulation in the expressions of Bax and Apaf-1 as well as down-regulation in the expression of Bcl-2 was observed. The time course change of ROS was prior to the changes of above investigated indexes. All of these results strongly suggest that EMAP II could induce rat C6 glioma cells apoptosis via the mitochondria( pathway, and ROS, Bax/Bcl-2 might be involved in this processing. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码：595 / 601
页数：7
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