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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.
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页码:1925 / 1933
页数:9
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