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题名: Neoalbaconol induces cell death through necroptosis by regulating RIPK-dependent autocrine TNF alpha and ROS production
作者: Yu, Xinfang1, 2, 3; Deng, Qipan1, 2, 3; Li, Wei1, 2, 3; Xiao, Lanbo1, 2, 3; Luo, Xiangjian1, 2, 3; Liu, Xiaolan1, 2, 3; Yang, Lifang1, 2, 3; Peng, Songling1, 2, 3; Ding, Zhihui4; Feng, Tao4; Zhou, Jian6; Fan, Jia6; Bode, Ann M.5; Dong, Zigang5; null(刘吉开)4; Cao, Ya1, 2, 3
刊名: ONCOTARGET
出版日期: 2015-02-10
卷号: 6, 期号:4, 页码:1995-2008
关键词: necoalbaconol ; necroptosis ; RIPK ; TNF alpha ; NF-kappa B signaling pathway ; ROS
学科分类: Oncology; Cell Biology
通讯作者: Liu,JK (reprint author),Chinese Acad Sci,Kunming Inst Bot,State Key Lab Phytochem & Plant Resources West Ch,Beijing 100864,Yunnan,Peoples R China. ; jkliu@mail.kib.ac.cn ; ycao98@vip.sina.com
文章类型: Article
英文摘要: Necroptosis/regulated necrosis is a caspase-independent, but receptor interacting protein kinase (RIPK)-dependent form of cell death. In previous studies, neoalbaconol (NA), a constituent extracted from Albatrellus confluens, was demonstrated to induce necroptosis in some cancer cell lines. The molecular mechanism of NA-induced necroptosis is described in this research study. We determined that NA-induced cell death is partly dependent on tumor necrosis factor a (TNF alpha) feed-forward signaling. More importantly, NA abolished the ubiquitination of RIPK1 by down-regulating E3 ubiquitin ligases, cellular inhibitors of apoptosis protein 1/2 (cIAP1/2) and TNF alpha receptor-associated factors (TRAFs). The suppression of RIPK1 ubiquitination induced the activation of the non-canonical nuclear factor-kappa B (NF-kappa B) pathway and stimulated the transcription of TNF alpha. Moreover, we also found that NA caused RIPK3-mediated reactive oxygen species (ROS) production and contribution to cell death. Taken together, these results suggested that two distinct mechanisms are involved in NA-induced necroptosis and include RIPK1/NF-kappa B-dependent expression of TNF alpha and RIPK3-dependent generation of ROS.
类目[WOS]: Oncology ; Cell Biology
研究领域[WOS]: Oncology ; Cell Biology
关键词[WOS]: NF-KAPPA-B ; MIXED LINEAGE KINASE ; APOPTOSIS RESISTANCE ; SIGNALING PATHWAY ; CANCER-CELLS ; NECROSIS ; ACTIVATION ; CIAP1 ; AGENTS ; MANNER
收录类别: SCI
项目资助者: National Key Basic Research Program of China [2009CB522300, 2011CB504305] ; State Key Program of National Natural Science Foundation of China [81430064] ; Hunan Provincial Innovation Foundation for Postgraduate [CX2012B082]
语种: 英语
WOS记录号: WOS:000352691800008
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内容类型: 期刊论文
URI标识: http://ir.kib.ac.cn/handle/151853/20623
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

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作者单位: 1.Cent S Univ, Xiangya Sch Med, Canc Res Inst, Changsha, Hunan, Peoples R China
2.Cent S Univ, Chinese Minist Educ, Key Lab, Changsha, Hunan, Peoples R China
3.Cent S Univ, Chinese Minist Publ Hlth, Key Lab Carcinogenesis, Changsha, Hunan, Peoples R China
4.Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem & Plant Resources West Ch, Beijing 100864, Yunnan, Peoples R China
5.Univ Minnesota, Hormel Inst, Austin, MN 55912 USA
6.Zhongshan Hosp, Liver Surg Dept, Liver Canc Inst, Shanghai, Peoples R China
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