中国科学院昆明植物研究所机构知识库
Advanced  
KIB OpenIR  > 植物化学与西部植物资源持续利用国家重点实验室  > 期刊论文
题名: Grifolin, a potent antitumour natural product upregulates death-associated protein kinase 1 DAPK1 via p53 in nasopharyngeal carcinoma cells
作者: Luo, Xiang-jian1; Li, Li-li1; Deng, Qi-pan1; Yu, Xin-fang1; Yang, Li-fang1; Luo, Fei-jun1; Xiao, Lan-bo1; Chen, Xiao-yan1; Ye, Mao1; Liu, Ji-kai2; Cao, Ya1
刊名: EUROPEAN JOURNAL OF CANCER
关键词: Grifolin ; Mushroom ; DAPK1 ; p53 ; Apoptosis
英文摘要: Grifolin, a secondary metabolite isolated from the fresh fruiting bodies of the mushroom Albatrellus confluens, has been shown to inhibit the growth of some cancer cell lines in vitro by induction of apoptosis in previous studies of our group. However, the mechanisms of action are not completely understood. An apoptosis-related gene expression profiling analysis provided a clue that death-associated protein kinase 1 (dapk1) gene was upregulated at least twofold in response to grifolin treatment in nasopharyngeal carcinoma cell CNE1. Here, we further investigated the role of DAPK1 in apoptotic effect induced by grifolin. We observed that protein as well as mRNA level of DAPK1 was induced by grifolin in a dose-dependent manner in nasopharyngeal carcinoma cell CNE1. We found that grifolin increased both Ser392 and Ser20 phosphorylation levels of transcription factor p53 protein, which could promote its transcriptional activity. Moreover, induced by grifolin, the recruitment of p53 to dapk1 gene promoter was confirmed to enhance markedly using EMSA and ChIP assays analysis. The involvement of DAPK1 in grifolin-induced apoptosis was supported by the studies that introducing siRNA targeting DAPK1 to CNE1 cells remarkably interfered grifolin-caused apoptotic effect as well as the activation of caspase-3. Grifolin induced upregulation of DAPK1 via p53 was also observed in tumour cells derived from human breast cancer and human colon cancer. The findings suggest that upregulation of DAPK1 via p53-DAPK1 pathway is an important mechanism of grifolin contributing to its ability to induce apoptotic effect. Since growing evidence found a significant loss of DAPK1 expression in a large variety of tumour types, grifolin may represent a promising candidate in the intervention of cancer via targeting DAPK1. (C) 2010 Elsevier Ltd. All rights reserved.
出版日期: 2011
卷号: 47, 期号:2, 页码:316-325
DOI标识: 10.1016/j.ejca.2010.09.021
语种: 英语
收录类别: SCI
学科分类: Oncology
ISSN号: 0959-8049
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.kib.ac.cn/handle/151853/5329
Appears in Collections:植物化学与西部植物资源持续利用国家重点实验室_期刊论文

Files in This Item: Download All
File Name/ File Size Content Type Version Access License
201204050010.pdf(1466KB)----开放获取--View Download

作者单位: 1.Cent S Univ, Xiangya Sch Med, Canc Res Inst, Changsha 410078, Hunan, Peoples R China
2.Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem & Plant Resource W China, Kunming 650204, Yunnan, Peoples R China

Recommended Citation:
Luo, XJ; Li, LL; Deng, QP; Yu, XF; Yang, LF; Luo, FJ; Xiao, LB; Chen, XY; Ye, M; Liu, JK; Cao, Y.Grifolin, a potent antitumour natural product upregulates death-associated protein kinase 1 DAPK1 via p53 in nasopharyngeal carcinoma cells,EUROPEAN JOURNAL OF CANCER,2011,47(2):316-325
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Luo, Xiang-jian]'s Articles
[Li, Li-li]'s Articles
[Deng, Qi-pan]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Luo, Xiang-jian]‘s Articles
[Li, Li-li]‘s Articles
[Deng, Qi-pan]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit
文件名: 201204050010.pdf
格式: Adobe PDF
此文件暂不支持浏览
所有评论 (0)
暂无评论
 
评注功能仅针对注册用户开放,请您登录
您对该条目有什么异议,请填写以下表单,管理员会尽快联系您。
内 容:
Email:  *
单位:
验证码:   刷新
您在IR的使用过程中有什么好的想法或者建议可以反馈给我们。
标 题:
 *
内 容:
Email:  *
验证码:   刷新

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  中国科学院昆明植物研究所 - Feedback
Powered by CSpace