Eriocalyxin B induces apoptosis of t(8;21) leukemia cells through NF-kappa B and MAPK signaling pathways and triggers degradation of AML1-ETO oncoprotein in a caspase-3-dependent manner
文献类型:期刊论文
作者 | Wang, L.![]() |
刊名 | CELL DEATH AND DIFFERENTIATION
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出版日期 | 2007-02-01 |
卷号 | 14期号:2页码:306-317 |
关键词 | eriocalyxin B acute myeloid leukemia apoptosis NF-kappa B MAPK AML1-ETO |
ISSN号 | 1350-9047 |
通讯作者 | Sun, HD (reprint author), Shanghai Jiao Tong Univ, Rui Jin Hosp, Sch Med, Shanghai Inst Hematol,State Key Lab Med Genom, 197 Rui Jin Er Rd, Shanghai 200025, Peoples R China. hdsun@mail.kib.ac.cn ; sjchen@stn.sh.cn |
英文摘要 | Diterpenoids isolated from Labiatae family herbs have strong antitumor activities with low toxicity. In this study, Eriocalyxin B (EriB), a diterpenoid extracted from Isodon eriocalyx, was tested on human leukemia/lymphoma cells and murine leukemia models. Acute myeloid leukemia cell line Kasumi-1 was most sensitive to EriB. Significant apoptosis was observed, concomitant with Bcl-2/Bcl-X-L downregulation, mitochondrial instability and caspase-3 activation. AML1-ETO oncoprotein was degraded in parallel to caspase-3 activation. EriB-mediated apoptosis was associated with NF-kappa B inactivation by preventing NF-kappa B nuclear translocation and inducing I kappa B alpha cleavage, and disturbance of MAPK pathway by downregulating ERK1/2 phosphorylation and activating AP-1. Without affecting normal hematopoietic progenitor cells proliferation, EriB was effective on primary t(8; 21) leukemia blasts and caused AML1-ETO degradation. In murine t(8; 21) leukemia models, EriB remarkably prolonged the survival time or decreased the xenograft tumor size. Together, EriB might be a potential treatment for t(8; 21) leukemia by targeting AML1-ETO oncoprotein and activating apoptosis pathways. |
学科主题 | Biochemistry & Molecular Biology; Cell Biology |
类目[WOS] | Biochemistry & Molecular Biology ; Cell Biology |
研究领域[WOS] | Biochemistry & Molecular Biology ; Cell Biology |
关键词[WOS] | ACUTE MYELOGENOUS LEUKEMIA ; TRANSCRIPTION FACTORS ; RABDOSIA-RUBESCENS ; ORIDONIN ; DEATH ; CANCER ; ALPHA ; INHIBITION ; ACTIVATION ; MECHANISM |
收录类别 | SCI |
语种 | 英语 |
WOS记录号 | WOS:000243493000011 |
公开日期 | 2012-10-12 |
源URL | [http://ir.kib.ac.cn/handle/151853/15410] ![]() |
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.Shanghai Jiao Tong Univ, Rui Jin Hosp, Sch Med, Shanghai Inst Hematol,State Key Lab Med Genom, Shanghai 200025, Peoples R China 2.Shanghai Jiao Tong Univ, Inst Biol Sci, Inst Hlth Sci, Shanghai 200025, Peoples R China 3.Chinese Acad Sci, Grad Sch, Shanghai 200025, Peoples R China 4.Chinese Acad Sci, Kunming Int Bot, Kunming 650204, Yunnan, Peoples R China |
推荐引用方式 GB/T 7714 | Wang, L.,Zhao, W. -L.,Yan, J. -S.,et al. Eriocalyxin B induces apoptosis of t(8;21) leukemia cells through NF-kappa B and MAPK signaling pathways and triggers degradation of AML1-ETO oncoprotein in a caspase-3-dependent manner[J]. CELL DEATH AND DIFFERENTIATION,2007,14(2):306-317. |
APA | Wang, L..,Zhao, W. -L..,Yan, J. -S..,Liu, P..,Sun, H. -P..,...&Chen, S. -J..(2007).Eriocalyxin B induces apoptosis of t(8;21) leukemia cells through NF-kappa B and MAPK signaling pathways and triggers degradation of AML1-ETO oncoprotein in a caspase-3-dependent manner.CELL DEATH AND DIFFERENTIATION,14(2),306-317. |
MLA | Wang, L.,et al."Eriocalyxin B induces apoptosis of t(8;21) leukemia cells through NF-kappa B and MAPK signaling pathways and triggers degradation of AML1-ETO oncoprotein in a caspase-3-dependent manner".CELL DEATH AND DIFFERENTIATION 14.2(2007):306-317. |
入库方式: OAI收割
来源:昆明植物研究所
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