The mitogen-activated/extracellular signal-regulated kinase kinase 1/2 inhibitor U0126 induces glial fibrillary acidic protein expression and reduces the proliferation and migration of C6 glioma cells

被引:38
|
作者
Lind, C. R. P.
Gray, C. W.
Pearson, A. G.
Cameron, R. E.
O'Carroll, S. J.
Narayan, P. J.
Lim, J.
Dragunow, M.
机构
[1] Univ Auckland, Dept Pharmacol & Clin Pharmacol, Fac Med & Hlth Sci, Auckland 1, New Zealand
[2] Auckland City Hosp, Dept Neurosurg, Auckland, New Zealand
[3] Univ Auckland, Dept Anat Radiol, Fac Med & Hlth Sci, Auckland 1, New Zealand
[4] Univ Auckland, Fac Med & Hlth Sci, Nat Rse Ctr Growth & Dev, Auckland 1, New Zealand
关键词
glioma; glioblastoma; mitogen-activated protein kinase kinase; mitogen-activated protein kinase kinase inhibitors; U0126; glial fibrillary acidic protein;
D O I
10.1016/j.neuroscience.2006.05.038
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The extracellular signal-regulated kinase (ERK) signaling pathway has been implicated in diverse cellular functions. ERK and its activating kinase, mitogen-activated/extracellular signal-regulated kinase kinase (MEK), are downstream of cell surface receptors known to be up-regulated in many malignant gliomas. We sought to investigate the role of ERK in glioma cell migration, proliferation and differentiation using the rat-derived C6 glioma cell line and the MEK inhibitor, U0126. Treatment of C6 cells with U0126 caused a significant concentration-dependent reduction in cell proliferation and migration and also induced expression of glial fibrillary acidic protein, a marker of astrocytic differentiation. These results suggest that the ERK pathway regulates glioma cell proliferation, migration and differentiation. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:1925 / 1933
页数:9
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