Effect of bryostatin 1 on taxol-induced apoptosis and cytotoxicity in human leukemia cells (U937).
Effect of bryostatin 1 on taxol-induced apoptosis and cytotoxicity in human leukemia cells (U937).
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苔藓抑素 1 对紫杉醇诱导的人白血病细胞 (U937) 细胞凋亡和细胞毒性的影响。
DOI：
10.1016/s0006-2952(98)00188-9
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发表时间：
1998
影响因子：
5.8
通讯作者：
Grant,S
中科院分区：
文献类型：
--
作者：
Wang,S;Guo,CY;Castillo,A;Dent,P;Grant,S
We have examined the effects of the macrocyclic lactone protein kinase C (PKC) activator bryostatin 1 on taxol-induced apoptosis and inhibition of clonogenicity in the human monocytic leukemia cell line U937. Exposure of cells to bryostatin 1 (10 nM; 15 hr) after (but not before) a 6-hr incubation with 0.5 μM taxol significantly increased apoptosis and resulted in an approximately 3 log reduction in clonogenicity. Cell cycle analysis revealed that the increase in apoptotic cells following bryostatin 1 treatment occurred primarily in the population undergoing taxol-mediated G2M arrest. The actions of bryostatin 1 were not attributable to potentiation of taxol-induced tubulin stabilization or to a reduction in the intracellular retention of taxol. Following exposure of cells to taxol, the Bcl-2 protein displayed an alteration in mobility that was not modified appreciably by bryostatin 1 treatment. The mobility shift in Bcl-2 protein from cells exposed to taxol followed by bryostatin 1 was eliminated by treatment of lysates with the protein phosphatase 2A (PP2A); the latter effect was blocked by okadaic acid. Treatment of cells with taxol followed by bryostatin 1 did not increase the amount of total Bax (compared with treatment with taxol alone), but did increase the amount of free Bax in the supernatant fraction. Finally, the ability of bryostatin 1 to potentiate taxol-induced apoptosis in U937 cells was mimicked closely by 2′-amino-3′-methoxyflavone (PD98059), a specific inhibitor of the mitogen-activated protein kinase (MAPK) kinase (MEK). Collectively, these findings indicate that bryostatin 1 increases the susceptibility of U937 cells to taxol-induced apoptosis and inhibition of clonogenicity. They also raise the possibility that this phenomenon may involve functional alterations in Bcl-2 and/or other proteins involved in regulation of the cell death pathway.
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DOI：
--
发表时间：
1996
期刊：
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research
影响因子：
--
作者：
M. Sheikh;M. García;Q. Zhan;Y. Liu;A. Fornace
通讯作者：
A. Fornace
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影响因子：
5.8
作者：
Jarvis,WD;Povirk,LF;Turner,AJ;Traylor,RS;Gewirtz,DA;Pettit,GR;Grant,S
通讯作者：
Grant,S
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DOI：
--
发表时间：
1995
期刊：
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
影响因子：
--
作者：
Bhatia,U;Traganos,F;Darzynkiewicz,Z
通讯作者：
Darzynkiewicz,Z
DOI：
10.1016/s0021-9258(17)42143-0
发表时间：
1994-01
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Z. Szallasi;Colin B. Smith;G. Pettit;P. Blumberg
通讯作者：
Z. Szallasi;Colin B. Smith;G. Pettit;P. Blumberg
影响因子：
11.2
作者：
Richard B. Lock;L. Stribinskiene
通讯作者：
Richard B. Lock;L. Stribinskiene