Delayed Cell Cycle Progression and Apoptosis Induced by Hemicellulase-Treated Agaricus blazei.
Delayed Cell Cycle Progression and Apoptosis Induced by Hemicellulase-Treated Agaricus blazei.
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DOI：
10.1093/ecam/nel059
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发表时间：
2007-03
期刊：
影响因子：
--
通讯作者：
Kasai H
中科院分区：
文献类型：
--
作者：
Kawamura M;Kasai H
我们检测了经半纤维素酶处理的姬松茸(AB组分H，ABH)对几种肿瘤细胞系生长的影响。ABH对某些细胞株的增殖有抑制作用，但无细胞毒作用。显著延长细胞周期的S时相。ABH还可诱导不同细胞系线粒体介导的细胞凋亡。然而，它对其他细胞系的生长没有影响。ABH可诱导细胞内p38丝裂原活化蛋白激酶(MAPK)的强激活，从而诱导细胞凋亡。另一方面，ABH在那些延迟细胞周期进程的细胞株中只显示出微弱的p38激活作用，几乎没有诱导细胞凋亡。但p38MAPK特异性抑制剂可抑制ABH诱导的上述两种作用，而ABH在肿瘤坏死因子-α诱导的高p38MAPK活性条件下，也可诱导后者的细胞凋亡。这些结果表明，p38MAPK对ABH的反应性在不同的细胞系中是不同的，决定了随后的细胞对细胞生长的反应。
We examined the effects of hemicellulase-treated Agaricus blazei (AB fraction H, ABH) on growth of several tumor cell lines. ABH inhibited the proliferation of some cell lines without cytotoxic effects. It markedly prolonged the S phase of the cell cycle. ABH also induced mitochondria-mediated apoptosis in different cell lines. However, it had no impact on the growth of other cell lines. ABH induced strong activation of p38 mitogen-activated protein kinase (MAPK) in the cells in which it evoked apoptosis. On the other hand, ABH showed only a weak p38 activation effect in those cell lines in which it delayed cell cycle progression with little induction of apoptosis. However, p38 MAPK-specific inhibitor inhibited both ABH-induced effects, and ABH also caused apoptosis in the latter cells under conditions of high p38 MAPK activity induced by combined treatment with TNF-α. These results indicate that the responsiveness of p38 MAPK to ABH, which differs between cell lines, determines subsequent cellular responses on cell growth.
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影响因子：
5.3
作者：
Benhar, M;Dalyot, I;Levitzki, A
通讯作者：
Levitzki, A
影响因子：
56.9
作者：
HAN, J;LEE, JD;ULEVITCH, RJ
通讯作者：
ULEVITCH, RJ
影响因子：
3.2
作者：
Bellini, MF;Angeli, JPF;Mantovani, MS
通讯作者：
Mantovani, MS
DOI：
10.1023/a:1008054111445
发表时间：
1998-01-01
期刊：
BIOTHERAPY
影响因子：
--
作者：
Ebina, T;Fujimiya, Y
通讯作者：
Fujimiya, Y
DOI：
10.1016/s1383-5718(01)00228-5
发表时间：
2001-09-20
影响因子：
1.9
作者：
Delmanto, RD;de Lima, PLA;Ribeiro, LR
通讯作者：
Ribeiro, LR