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 | |
刊名 | ONCOTARGET |
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 |
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 |
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. |
学科主题 | Oncology; Cell Biology |
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 |
语种 | 英语 |
WOS记录号 | WOS:000352691800008 |
公开日期 | 2015-07-07 |
内容类型 | 期刊论文 |
源URL | [http://ir.kib.ac.cn/handle/151853/20623] |
专题 | 昆明植物研究所_植物化学与西部植物资源持续利用国家重点实验室 |
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 |
推荐引用方式 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.,...&Cao, Ya.(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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