Comparison between cells and cancer stem-like cells isolated from glioblastoma and astrocytoma on resistance-associated protein genes

被引:59
作者
Jin, F. [2 ]
Zhao, L. [1 ]
Zhao, H. -Y. [2 ]
Guo, S. -G. [3 ]
Feng, J. [2 ]
Jiang, X. -B. [2 ]
Zhang, S. -L. [1 ]
Wei, Y. J. [2 ]
Fu, R. [2 ]
Zhao, J. -S. [2 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Hepatol & Infect Dis, Wuhan 430022, Peoples R China
[2] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Neurosurg, Wuhan 430022, Peoples R China
[3] Shandong Prov Hosp, Dept Neurol, Jinan 250021, Peoples R China
关键词
glioma; cancer stem-like cell; glioblastoma; astrocytoma; livin; multidrug resistance-associated protein;
D O I
10.1016/j.neuroscience.2008.03.054
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
This study is to explore and compare the features of the cells and cancer stem-like cells (CSCs) isolated from both glioblastoma and astrocytoma on expression of anti-apoptotic and multidrug resistance-associated protein (MRP) genes. As a result, the mRNA expression of livin, livin alpha and MRP1 was up-regulated in human CSCs from 2 times to 85 times, but the gene expression of MRP3 was down-regulated from 0.09 times to 0.5 times. After just differentiation the mRNA expression of livin, livina and MRP3 was up-regulated from9 times to 64 times, but the mRNA expression of MRP1 was down-regulated from 0.01 times to 0.03 times. It is a rare report that glioma stem-like cells can be induced successfully from a grade 2-3 astrocytoma tissue. The properties of glioblastoma and astrocytoma stem-like cells on anti-apoptotic and MRP genes are: anti-apoptotic gene livin and survivin are elevated in CSCs but are the most increased in just differentiated CSCs; MRP1 gene is significantly increased and MRP3 is decreased in CSCs, but when differentiating the MRP3 gene starts a remarkable increase in CSCs; the expression of anti-apoptotic and MRP genes shows no differences between the CSCs isolated from glioblastoma and astrocytoma tissues. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:541 / 550
页数:10
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