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The p53 pathway is synergized by p38 mapk signaling to mediate 11,11 '-dideoxyverticillin-induced g(2)/m arrest

文献类型:期刊论文

作者Chen, Y; Miao, ZH; Zhao, WM; Ding, J
刊名Febs letters
出版日期2005-07-04
卷号579期号:17页码:3683-3690
ISSN号0014-5793
关键词11,11 '-dideoxyverticillin G(2)/m arrest P53 P38 mapk Chk2 Anti-tumor Hct-116 cell
DOI10.1016/j.febslet.2005.05.053
通讯作者Ding, j()
英文摘要The phytochemical 11,11'-dideoxyverticillin, derived from the fungus shiraia bambusicola, has been shown to possess potent anticancer activity in vitro and in vivo. here, we investigated the effect of 11,11'-dideoxyverticillin on cell cycle progression, and explored the potential mechanisms for this effect. a concentration- and time-dependent cell cycle blockade at g(2)/m phase was observed in human colon cancer cells (hct-116) following 11,11'-dideoxyverticillin treatment and was associated with marked increases in levels of p53, phospho-p53(ser20) and phospho-chk2(thr 68). when wild type p53 expression was specifically inhibited by rna interference, hct-116 cells treated with 11,11'-dideoxyverticillin failed to arrest in g2/m and did not show increased phospho-chk2(thr 68). on the other hand, 11,11'-dideoxyverticillin treatment also elicited p38 map kinase activity and expression of phospho-p38 mapk. treatment with a specific p38 mapk inhibitor (sb203580) successfully inhibited p38 mapk and delayed the onset of g2/m arrest induced by 0.5 mu m 11,11'-dideoxyverticillin after approximately 6h, but did not abolish the induction of g2/m arrest. additionally, sb203580 did not alter the levels of p53, phospho-p53 (ser20), or phospho-chk2 (thr68) proteins in 11,11'-dideoxyverticillin-treated cells. together, these findings indicate that p53-mediated phosphorylation of chk2 maybe plays a vital role in 11, 11-dideoxyverticillin-induced g arrest, and that p38 mapk might accelerate this progression. our work suggests a new possibility of interactions among p53, chk2 and p38 mapk signaling in g(2)/m arrest. (c) 2005 federation of european biochemical societies. published by elsevier b.v. all rights reserved.
WOS关键词CELL-CYCLE CHECKPOINTS ; DNA-DAMAGE CHECKPOINT ; INDUCED PHOSPHORYLATION ; PROTEIN-KINASE ; RADIATION ; CHK2 ; ACTIVATION ; GROWTH ; CANCER ; G(1)
WOS研究方向Biochemistry & Molecular Biology ; Biophysics ; Cell Biology
WOS类目Biochemistry & Molecular Biology ; Biophysics ; Cell Biology
语种英语
出版者ELSEVIER SCIENCE BV
WOS记录号WOS:000230335600034
URI标识http://www.irgrid.ac.cn/handle/1471x/2377289
专题中国科学院大学
通讯作者Ding, J
作者单位1.Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Mat Med, Div Anti Tumor Pharmacol,State Key Lab Drug Res, Shanghai, Peoples R China
2.Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Mat Med, Dept Phytochem, Shanghai, Peoples R China
3.Chinese Acad Sci, Grad Sch, Shanghai, Peoples R China
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GB/T 7714
Chen, Y,Miao, ZH,Zhao, WM,et al. The p53 pathway is synergized by p38 mapk signaling to mediate 11,11 '-dideoxyverticillin-induced g(2)/m arrest[J]. Febs letters,2005,579(17):3683-3690.
APA Chen, Y,Miao, ZH,Zhao, WM,&Ding, J.(2005).The p53 pathway is synergized by p38 mapk signaling to mediate 11,11 '-dideoxyverticillin-induced g(2)/m arrest.Febs letters,579(17),3683-3690.
MLA Chen, Y,et al."The p53 pathway is synergized by p38 mapk signaling to mediate 11,11 '-dideoxyverticillin-induced g(2)/m arrest".Febs letters 579.17(2005):3683-3690.

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来源:中国科学院大学

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