Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase pathway
Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase pathway
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Bex2 通过 c-Jun NH2 末端激酶途径调节恶性胶质瘤细胞的细胞增殖和凋亡。
DOI：
10.1016/j.bbrc.2012.09.100
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发表时间：
2012-10-26
影响因子：
3.1
通讯作者：
Yu, Rutong
中科院分区：
文献类型：
--
作者：
Zhou, Xiuping;Meng, Qingming;Yu, Rutong
Bex 2是脑表达X连锁基因家族的成员之一，其在胶质瘤中的功能存在争议，其机制在很大程度上是未知的。我们在这里报告，Bex 2调节恶性胶质瘤细胞的细胞增殖和凋亡通过c-Jun氨基末端激酶（JNK）途径。Bex 2在胶质瘤组织中的表达水平明显增高。我们观察到Bex 2的过表达促进细胞增殖，而Bex 2的下调抑制细胞生长。此外，Bex 2下调促进细胞凋亡并激活JNK通路;这些作用通过施用JNK特异性抑制剂SP 600125来消除。因此，Bex 2可能在胶质瘤的发生发展过程中起重要作用。(C)2012 Elsevier Inc. All rights reserved.
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.