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Mansouramycin C kills cancer cells through reactive oxygen species production mediated by opening of mitochondrial permeability transition pore
Kuang, Shan1,2; Liu, Ge1,2,3; Cao, Ruobing1,2,3; Zhang, Linlin1,2,3; Yu, Qiang4; Sun, Chaomin1,2
2017-11-28
Source PublicationONCOTARGET
Volume8Issue:61Pages:104057-104071
SubtypeArticle
AbstractCancer is one of the deadliest diseases in the world and the search for novel anticancer agents is urgently required. Marine-derived isoquinolinequinones have exhibited promising anticancer activities. However, the exact mechanisms of cytotoxic activities of these isoquinolinequinones are poorly characterized. In this study, we investigated the anticancer effects and molecular mechanisms of mansouramycin C (Mm C), a cytotoxic isoquinolinequinone isolated from a marine streptomycete. We demonstrated that Mm C preferentially killed cancer cells and the cytotoxic effects were mediated by reactive oxygen species (ROS) generation. Mass spectrometry based proteomic analysis of Mm C-treated A549 cells revealed that many ROS-related proteins were differentially expressed. Proteomic-profiling after Mm C treatment identified oxidative phosphorylation as the most significant changes in pathways. Analysis also revealed extensive defects in mitochondrial structure and function. Furthermore, we disclosed that Mm C-induced ROS generation was caused by opening of mitochondrial permeability transition pore. Notably, Mm C synergized with sorafenib to induce cell death in A549 cells. Hence, we propose that the marine-derived natural compound Mm C is a potent inducer of the mitochondrial permeability transition and a promising anticancer drug candidate. Moreover, molecular mechanisms of Mm C shed new light on the understanding of the cytotoxic mechanisms of marine-derived isoquinolinequiones.
KeywordMansouramycin c Marine-derived Isoquinolinequinone Reactive Oxygen Species Mitochondrial Permeability Transition Pore Anticancer Drug
DOI10.18632/oncotarget.22004
Indexed BySCI
Language英语
WOS IDWOS:000419562500104
Citation statistics
Cited Times:4[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Version出版稿
Identifierhttp://ir.qdio.ac.cn/handle/337002/154342
Collection实验海洋生物学重点实验室
Affiliation1.Chinese Acad Sci, Inst Oceanol, Key Lab Expt Marine Biol, Qingdao, Peoples R China
2.Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao, Peoples R China
3.Univ Chinese Acad Sci, Coll Earth Sci, Beijing, Peoples R China
4.Chinese Acad Sci, Shanghai Inst Mat Med, Div Tumor Pharmacol, Shanghai, Peoples R China
First Author AffilicationInstitute of Oceanology, Chinese Academy of Sciences
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GB/T 7714
Kuang, Shan,Liu, Ge,Cao, Ruobing,et al. Mansouramycin C kills cancer cells through reactive oxygen species production mediated by opening of mitochondrial permeability transition pore[J]. ONCOTARGET,2017,8(61):104057-104071.
APA Kuang, Shan,Liu, Ge,Cao, Ruobing,Zhang, Linlin,Yu, Qiang,&Sun, Chaomin.(2017).Mansouramycin C kills cancer cells through reactive oxygen species production mediated by opening of mitochondrial permeability transition pore.ONCOTARGET,8(61),104057-104071.
MLA Kuang, Shan,et al."Mansouramycin C kills cancer cells through reactive oxygen species production mediated by opening of mitochondrial permeability transition pore".ONCOTARGET 8.61(2017):104057-104071.
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