Mansouramycin C kills cancer cells through reactive oxygen species production mediated by opening of mitochondrial permeability transition pore
文献类型：期刊论文
| 作者 | Kuang, Shan1,2; Liu, Ge1,2,3; Cao, Ruobing1,2,3; Zhang, Linlin1,2,3; Yu, Qiang4; Sun, Chaomin1,2 |
| 刊名 | ONCOTARGET
 |
| 出版日期 | 2017-11-28 |
| 卷号 | 8期号:61页码:104057-104071 |
| 关键词 | Mansouramycin c Marine-derived Isoquinolinequinone Reactive Oxygen Species Mitochondrial Permeability Transition Pore Anticancer Drug |
| DOI | 10.18632/oncotarget.22004 |
| 文献子类 | Article |
| 英文摘要 | Cancer 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. |
| 语种 | 英语 |
| WOS记录号 | WOS:000419562500104 |
| 版本 | 出版稿 |
| 源URL | [http://ir.qdio.ac.cn/handle/337002/154342]  |
| 专题 | 海洋研究所_实验海洋生物学重点实验室 |
| 作者单位 | 1.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 |
| 推荐引用方式 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. |
入库方式： OAI收割
来源：海洋研究所
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