Acquisition of temozolomide resistance by the rat C6 glioma cell line increases cell migration and side population phenotype
Acquisition of temozolomide resistance by the rat C6 glioma cell line increases cell migration and side population phenotype
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大鼠 C6 神经胶质瘤细胞系获得替莫唑胺耐药性会增加细胞迁移和侧群表型
DOI：
10.3892/or.2019.7350
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发表时间：
2019-10
期刊：
影响因子：
4.2
通讯作者：
Li Jiejing
中科院分区：
文献类型：
--
作者：
Xu Ya;Yang Xiangcai;Mei Shuting;Sun Yi;Li Jiejing
据报道，肿瘤干细胞与胶质瘤的耐药有关，但关于肿瘤干细胞对耐药的影响，研究结果相互矛盾。本研究的目的是通过Transwell侵袭试验、流式细胞术和western blot分析以及免疫组织化学染色，确定大鼠C6胶质瘤细胞耐药的潜在机制。结果表明，C6细胞获得耐药性增强了体内和体外的迁移能力。值得注意的是，耐药并不依赖于C6细胞的癌症干细胞，而是依赖于侧群表型的增加。阻断ABC转运蛋白可增加替莫唑胺对C6细胞的敏感性和替莫唑胺诱导的细胞凋亡。总的来说，这些数据表明C6细胞的耐药是由侧群体表型介导的，而不是由癌症干细胞介导的。
Cancer stem cells are reportedly associated with drug resistance in glioma, but there are conflicting findings on the effects of cancer stem cells on drug resistance. The aim of the present study was to identify the underlying mechanisms of drug resistance in rat C6 glioma cells, through the use of Transwell invasion assays, flow cytometric and western blot analyses as well as immunohistochemical staining. The results revealed that acquisition of drug resistance by C6 cells enhanced migration ability in vivo and in vitro. Notably, drug resistance did not depend on the cancer stem cells of C6 cells, but on the increase of a side population phenotype. Blockade of the ABC transporter could increase sensitivity to temozolomide and temozolomide-induced apoptosis in C6 cells. Collectively, these data indicated that drug resistance of C6 cells was mediated by the side population phenotype rather than by cancer stem cells.
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影响因子：
64.5
作者：
Kim J;Woo AJ;Chu J;Snow JW;Fujiwara Y;Kim CG;Cantor AB;Orkin SH
通讯作者：
Orkin SH
DOI：
--
发表时间：
2009
期刊：
--
影响因子：
--
作者：
Xiaowei Sun;R. Essalmani;N. Seidah;A. Prat
通讯作者：
Xiaowei Sun;R. Essalmani;N. Seidah;A. Prat
影响因子：
5.7
作者：
Neradil J;Veselska R
通讯作者：
Veselska R
DOI：
10.1038/nrd4461
发表时间：
2015-01
期刊：
Nature reviews. Drug discovery
影响因子：
--
作者：
Nigam SK
通讯作者：
Nigam SK
影响因子：
7.3
作者：
Burkert, J.;Otto, W. R.;Wright, N. A.
通讯作者：
Wright, N. A.