Neoalbaconol induces cell death through necroptosis by regulating RIPK-dependent autocrine TNF alpha and ROS production
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; Liu, Jikai4; Cao, Ya1,2,3; 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
2015-02-10
Source PublicationONCOTARGET
Volume6Issue:4Pages:1995-2008
AbstractNecroptosis/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.
KeywordNecoalbaconol Necroptosis Ripk Tnf Alpha Nf-kappa b Signaling Pathway Ros
Subject AreaOncology ; Cell Biology
Indexed BySCI
Language英语
WOS Research AreaOncology ; Cell Biology
WOS SubjectOncology ; Cell Biology
WOS IDWOS:000352691800008
Citation statistics
Cited Times:48[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.kib.ac.cn/handle/151853/20623
Collection植物化学与西部植物资源持续利用国家重点实验室
Corresponding AuthorLiu,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
Affiliation1.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
Recommended Citation
GB/T 7714
Yu, Xinfang,Deng, Qipan,Li, Wei,et al. Neoalbaconol induces cell death through necroptosis by regulating RIPK-dependent autocrine TNF alpha and ROS production[J]. ONCOTARGET,2015,6(4):1995-2008.
APA Yu, Xinfang.,Deng, Qipan.,Li, Wei.,Xiao, Lanbo.,Luo, Xiangjian.,...&ycao98@vip.sina.com.(2015).Neoalbaconol induces cell death through necroptosis by regulating RIPK-dependent autocrine TNF alpha and ROS production.ONCOTARGET,6(4),1995-2008.
MLA Yu, Xinfang,et al."Neoalbaconol induces cell death through necroptosis by regulating RIPK-dependent autocrine TNF alpha and ROS production".ONCOTARGET 6.4(2015):1995-2008.
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