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 |
| 关键词 | 11,11 '-dideoxyverticillin G(2)/M arrest p53 p38 MAPK Chk2 anti-tumor HCT-116 cell |
| ISSN号 | 0014-5793 |
| DOI | 10.1016/j.febslet.2005.05.053 |
| 文献子类 | Article |
| 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 |
| 语种 | 英语 |
| WOS记录号 | WOS:000230335600034 |
| 出版者 | ELSEVIER SCIENCE BV |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/273836]  |
| 专题 | 药理学第一研究室 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
| 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 |
| 推荐引用方式 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. |
入库方式： OAI收割
来源：上海药物研究所
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