Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase pathway

被引：29

作者：

Zhou, Xiuping ^{[1
,2
,3
]}

Meng, Qingming ^{[1
,4
]}

Xu, Xuebin ^{[4
]}

Zhi, Tongle ^{[4
]}

Shi, Qiong ^{[1
,2
,3
]}

Wang, Yong ^{[4
]}

Yu, Rutong ^{[1
,2
,3
]}

机构：

[1] Xuzhou Med Coll, Affiliated Hosp, Dept Neurosurg, Xuzhou 221002, Jiangsu, Peoples R China

[2] Xuzhou Med Coll, Lab Neurosurg, Xuzhou 221002, Jiangsu, Peoples R China

[3] Xuzhou Med Coll, Affiliated Hosp, Key Lab Brain Dis Biol, Xuzhou 221002, Jiangsu, Peoples R China

[4] Xuzhou Med Coll, Grad Sch, Xuzhou 221002, Jiangsu, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2012年 / 427卷 / 03期

基金：

中国国家自然科学基金;

关键词：

Glioma; Bex2; Proliferation; Apoptosis; JNK; N-TERMINAL KINASE; GENE FAMILY; NEUROTROPHIN RECEPTOR; JNK; EXPRESSION; IDENTIFICATION; TUMORS;

D O I：

10.1016/j.bbrc.2012.09.100

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 function of Bex2, a member of the Brain Expressed X-linked gene family, in glioma is controversial and its mechanism is largely unknown. We report here that Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase (JNK) pathway. The expression level of Bex2 is markedly increased in glioma tissues. We observed that Bex2 over-expression promotes cell proliferation, while down-regulation of Bex2 inhibits cell growth. Furthermore, Bex2 down-regulation promotes cell apoptosis and activates the JNK pathway; these effects were abolished by administration of the JNK specific inhibitor, SP600125. Thus, Bex2 may be an important player during the development of glioma. (C) 2012 Elsevier Inc. All rights reserved.

引用

页码：574 / 580

页数：7

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