The ability to survive mitosis in the presence of microtubule poisons differs significantly between human nontransformed (RPE-1) and cancer (U2OS, HeLa) cells.

The ability to survive mitosis in the presence of microtubule poisons differs significantly between human nontransformed (RPE-1) and cancer (U2OS, HeLa) cells.
复制标题

DOI:
10.1002/cm.20316
复制
发表时间:
2009-08
影响因子:
--
通讯作者:
Rieder, Conly L.
Rieder, Conly L.
中科院分区:
其他
文献类型:
--
作者:
Brito, Daniela A.;Rieder, Conly L.

文献摘要

参考文献

被引文献

相似文献

我们使用活细胞成像来比较人类非转化(RPE-1)和癌症(HeLa,U2 OS)细胞在诺考达唑或紫杉醇中进入有丝分裂时的命运。在同一视野中,在任一药物中,所有细胞系中的细胞均可能在有丝分裂中死亡,在10 h内退出有丝分裂并死亡,或退出有丝分裂并存活≥10 h。相对于RPE-1细胞,显著较少的HeLa或U2 OS细胞在有丝分裂中存活或在有丝分裂后保持活力:在抑制纺锤体微管组装的诺考达唑浓度下,或在500 nM紫杉醇中,分别有30%和27%的RPE-1细胞在退出有丝分裂10小时内死亡,而90%和49%的U2 OS以及78%和81%的HeLa细胞死亡。临床相关的紫杉醇浓度(5 nM)也是如此,与RPE-1细胞的1%相比,在有丝分裂或逃避有丝分裂的10小时内,分别杀死93%和46%的HeLa和U2 OS细胞。总之,这些数据表明,使用HeLa或U2 OS细胞的研究,收获后,在有丝分裂与诺考达唑或紫杉醇长时间的封锁,显着污染死亡或垂死的细胞。我们还发现,有丝分裂的持续时间和存活率之间的关系是药物和细胞类型特异性的,并且致死率与用于防止满足动粒附着检查点的细胞类型和药物有关。最后,使用pancaspase抑制剂的工作表明,在RPE-1细胞有丝分裂期间由诺考达唑触发的主要凋亡途径在U2 OS细胞中不活跃。细胞动力。Cytoskeleton 2008.
We used live cell imaging to compare the fate of human nontransformed (RPE-1) and cancer (HeLa, U2OS) cells as they entered mitosis in nocodazole or taxol. In the same field, and in either drug, a cell in all lines could die in mitosis, exit mitosis and die within 10 h, or exit mitosis and survive ≥10 h. Relative to RPE-1 cells, significantly fewer HeLa or U2OS cells survived mitosis or remained viable after mitosis: in nocodazole concentrations that inhibit spindle microtubule assembly, or in 500 nM taxol, 30% and 27% of RPE-1 cells, respectively, died in or within 10 h of exiting mitosis while 90% and 49% of U2OS and 78% and 81% of HeLa died. This was even true for clinically relevant taxol concentrations (5 nM) which killed 93% and 46%, respectively, of HeLa and U2OS cells in mitosis or within 10 h of escaping mitosis, compared to 1% of RPE-1 cells. Together these data imply that studies using HeLa or U2OS cells, harvested after a prolonged block in mitosis with nocodazole or taxol, are significantly contaminated with dead or dying cells. We also found that the relationship between the duration of mitosis and survival is drug and cell type specific and that lethality is related to the cell type and drug used to prevent satisfaction of the kinetochore attachment checkpoint. Finally, work with a pancaspase inhibitor suggests that the primary apoptotic pathway triggered by nocodazole during mitosis in RPE-1 cells is not active in U2OS cells. Cell Motil. Cytoskeleton 2008.
DOI: 10.1083/jcb.127.3.789
发表时间: 1994-11
期刊: The Journal of cell biology
影响因子: --
作者:
Andreassen PR;Margolis RL
通讯作者: Margolis RL
DOI: 10.1128/mcb.25.21.9232-9248.2005
发表时间: 2005-11-01
影响因子: 5.3
作者:
Kim, M;Murphy, K;Kao, GD
通讯作者: Kao, GD
DOI: 10.1126/science.7871434
发表时间: 1995-03-03
期刊: SCIENCE
影响因子: 56.9
作者:
CROSS, SM;SANCHEZ, CA;REID, BJ
通讯作者: REID, BJ
DOI: 10.1016/s0002-9440(10)63470-0
发表时间: 2003-09-01
影响因子: 6
作者:
Masuda, A;Maeno, K;Takahashi, T
通讯作者: Takahashi, T
DOI: 10.1038/32688
发表时间: 1998-03-19
期刊: NATURE
影响因子: 64.8
作者:
Cahill, DP;Lengauer, C;Vogelstein, B
通讯作者: Vogelstein, B