Anesthetic pentobarbital inhibits proliferation and migration of malignant glioma cells

被引：30

作者：

Xie, Jun ^{[1
]}

Li, Yan ^{[1
]}

Huang, Yijun ^{[1
]}

Qiu, Pengxin ^{[1
]}

Shu, Minfeng ^{[1
]}

Zhu, Wenbo ^{[1
]}

Ou, Yanqiu ^{[1
]}

Yan, Guangmei ^{[1
]}

机构：

[1] Sun Yat Sen Univ, Dept Pharmacol, Zhongshan Sch Med, Guangzhou 510089, Guangdong, Peoples R China

来源：

CANCER LETTERS | 2009年 / 282卷 / 01期

基金：

中国国家自然科学基金;

关键词：

Pentobarbital; Malignant glioma; Proliferation; Migration; Cell cycle; MAPK; HIGH-GRADE GLIOMA; BRAIN-TUMOR; GLIOBLASTOMA CELLS; RADIATION-THERAPY; CANCER-CELLS; IN-VITRO; MICROTUBULES; EFFICACY; POLYMERIZATION; TEMOZOLOMIDE;

D O I：

10.1016/j.canlet.2009.02.055

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Malignant gliomas are common and aggressive brain tumors in adults. The rapid proliferation and diffuse brain migration are main obstacles to successful treatment. Here we show that pentobarbital, a central depressant introduced clinically a century ago, is capable of suppressing proliferation and migration of C6 malignant glioma cells in a concentration-dependent manner. Pentobarbital also leads to a G1 phase cell cycle arrest accompanied by suppressed G1 cell cycle regulatory proteins Cyclin D1, Cyclin D3, CDK2 and phosphorylated Rb. In addition, noticeable morphological changes and interrupted alpha-tubulin microtubule assembly are induced by pentobarbital exposure. Intracellular signal pathways involved in the effect of pentobarbital is concerned with inactivation of ERK, c-Jun and Akt. Together, these findings suggest anti-proliferation and anti-migration effects of pentobarbital on malignant gliomas, most likely by arresting cell cycle and interfering microtubule. ERK, c-Jun MAPK and PI3K/Akt are possible signaling pathways involved. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

引用

页码：35 / 42

页数：8

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