共 45 条
DECREASED CCAAT/ENHANCER BINDING PROTEIN β EXPRESSION INHIBITS THE GROWTH OF GLIOBLASTOMA CELLS
被引:32
作者:
Aguilar-Morante, D.
[1
,2
]
Cortes-Canteli, M.
[1
,2
]
Sanz-Sancristobal, M.
[1
,2
]
Santos, A.
[3
]
Perez-Castillo, A.
[1
,2
]
机构:
[1] Univ Autonoma Madrid, CSIC, Inst Invest Biomed, Madrid 28029, Spain
[2] Ctr Invest Biomed Red Enfermedades Neurodegenerat, Madrid 28029, Spain
[3] Univ Complutense Madrid, Fac Med, Dept Bioquim & Biol Mol, Madrid, Spain
来源:
关键词:
C/EBP beta;
glioblastoma;
invasion;
proliferation;
shRNA;
EXPERIMENTAL BRAIN-TUMORS;
C/EBP-BETA;
IN-VIVO;
SKIN TUMORIGENESIS;
MAMMARY-GLAND;
DIFFERENTIATION;
GLIOMA;
PROLIFERATION;
SURVIVAL;
INJURY;
D O I:
10.1016/j.neuroscience.2010.12.025
中图分类号:
Q189 [神经科学];
学科分类号:
071006 ;
摘要:
C/EBP beta is a leucine-zipper transcription factor implicated in the control of metabolism, development, cell differentiation, and proliferation. However, it remains unclear its role in tumor development. Here, we show that down-regulation of C/EBP beta by RNA interference inhibits proliferation in the GL261 murine glioblastoma cell line, induces an arrest of the cell cycle at the G0/G1 boundary, and diminishes their transformation capacity and migration. In addition, we show that C/EBP beta regulates the expression of several DNA damage response- and invasion-related genes. Lastly, C/EBP beta depletion significantly retards tumor onset and prolongs survival in a murine orthotopic brain tumor model. Immunohistochemical analysis revealed a significant diminution of proliferating cell nuclear antigen (PCNA) labeling in tumors derived from C/EBP beta-depleted GL261 cells compared with that in controls. These results show, for the first time, the dependence of glioma cells on C/EBP beta and suggest a potential role of this transcription factor in glioma development. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
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页码:110 / 119
页数:10
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