Tanshinone-1 induces tumor cell killing, enhanced by inhibition of secondary activation of signaling networks
文献类型:期刊论文
作者 | Xu, L.1; Feng, J-M1; Li, J-X1; Zhu, J-M1; Song, S-S1; Tong, L-J1; Chen, Y.1; Yang, X-Y1; Shen, Y-Y1; Lian, F-L2 |
刊名 | CELL DEATH & DISEASE |
出版日期 | 2013-11 |
卷号 | 4 |
ISSN号 | 2041-4889 |
关键词 | tanshinone-1 multidrug resistance Stat3 p38 AKT ERK |
DOI | 10.1038/cddis.2013.443 |
文献子类 | Article |
英文摘要 | Tumor multidrug resistance (MDR) can result from overexpression of drug transporters and deregulation of cellular signaling transduction. New agents and strategies are required for overcoming MDR. Here, we report that tanshinone-1, a bioactive ingredient in traditional Chinese medicine, directly killed MDR tumor cells and their corresponding parental cells, which was potentiated by inhibition of secondary activation of signaling networks. Tanshinone-1 was slightly more potent at inducing cytotoxicity and apoptosis in MDR cells than in corresponding parental cells. Tanshinone-1-induced MDR cell killing was independent of the function and expression of drug transporters but was partially correlated with the phosphatase-dependent reduction of phospho-705-Stat3, which secondarily activated p38-, AKT-, and ERK-involved signaling networks. Cotreatments with p38, AKT, and ERK inhibitors potentiated the anti-MDR effects of tanshinone-1. Our study presents a model for MDR cell killing using a compound of natural origin. This model could lead to new therapeutic strategies for targeting signaling network(s) in MDR cancers as well as new strategies for multitarget design. |
WOS关键词 | HEPATOCELLULAR-CARCINOMA CELLS ; GROWTH-FACTOR RECEPTOR ; BREAST-CANCER CELLS ; MULTIDRUG-RESISTANCE ; APOPTOSIS INDUCTION ; KINASE INHIBITORS ; DRUG DISCOVERY ; LUNG-CANCER ; STAT3 ; EXPRESSION |
资助项目 | National Natural Science Foundation of China (NSFC)[81025020] ; National Natural Science Foundation of China (NSFC)[81202547] ; National Natural Science Foundation of China (NSFC)[81021062] ; National Basic Research Program of China[2012CB932502] ; National Science & Technology Major Project of China[2012ZX09301-001-002] ; 'Interdisciplinary Cooperation Team' Program for Science and Technology Innovation of the Chinese Academy of Sciences[00000000] ; Science and Technology Commission of Shanghai Municipality (STCSM)[13XD1404200] ; State Key Laboratory of Drug Research[00000000] |
WOS研究方向 | Cell Biology |
语种 | 英语 |
出版者 | NATURE PUBLISHING GROUP |
WOS记录号 | WOS:000327760500003 |
源URL | [http://119.78.100.183/handle/2S10ELR8/277392] |
专题 | 药物制剂研究中心 中科院受体结构与功能重点实验室 新药研究国家重点实验室 药物化学研究室 药理学第一研究室 国家新药筛选中心 |
通讯作者 | Li, Y-P |
作者单位 | 1.Chinese Acad Sci, Shanghai Inst Mat Med, State Key Lab Drug Res, Div Antitumor Pharmacol, Shanghai 201203, Peoples R China; 2.Chinese Acad Sci, Shanghai Inst Mat Med, NMR Lab, Shanghai 201203, Peoples R China |
推荐引用方式 GB/T 7714 | Xu, L.,Feng, J-M,Li, J-X,et al. Tanshinone-1 induces tumor cell killing, enhanced by inhibition of secondary activation of signaling networks[J]. CELL DEATH & DISEASE,2013,4. |
APA | Xu, L..,Feng, J-M.,Li, J-X.,Zhu, J-M.,Song, S-S.,...&Miao, Z-H.(2013).Tanshinone-1 induces tumor cell killing, enhanced by inhibition of secondary activation of signaling networks.CELL DEATH & DISEASE,4. |
MLA | Xu, L.,et al."Tanshinone-1 induces tumor cell killing, enhanced by inhibition of secondary activation of signaling networks".CELL DEATH & DISEASE 4(2013). |
入库方式: OAI收割
来源:上海药物研究所
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