| Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced chemokine release in both TRAIL-resistant and TRAIL-sensitive cells via nuclear factor kappa B. | |
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MedLine Citation:
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PMID: 19120450 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in a variety of tumour cells, but not in most normal cells, and has attracted considerable attention for its potential use in cancer therapy. Recently, increasing evidence has shown that TRAIL is involved in inflammation, although much of this evidence is controversial. In this article, it is shown that TRAIL induces CXCL2, CCL4 and CCL20 secretion in a nuclear factor kappa B-dependent manner. The dominant negative constructs of tumour necrosis factor receptor-associated death domain protein (TRADD) and tumour necrosis factor receptor-associated factor 2 are unable to block TRAIL-induced chemokine up-regulation, and the dominant negative construct of TRADD may even enhance TRAIL-triggered signals. Using small interfering RNA, receptor interacting protein has been demonstrated to be essential for TRAIL-induced chemokine release. Furthermore, it has been demonstrated that p38 mitogen-activated protein kinase is involved in TRAIL-induced chemokine release without any effects on nuclear factor kappa B activation, suggesting that some unknown transcription factors may be activated by TRAIL. Using a xenograft tumour model, it has been illustrated that TRAIL can also induce chemokine release in vivo. Although these chemokines induced by TRAIL are inflammatory chemokines, their functions are not restricted to inflammation and require further examination. Our results indicate that attention should be paid to the side-effects of TRAIL treatment, not only in TRAIL-resistant but also in TRAIL-sensitive tumour cells. |
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Authors:
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Wanhu Tang; Weimin Wang; Yaxi Zhang; Shilian Liu; Yanxin Liu; Dexian Zheng |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-12-12 |
Journal Detail:
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Title: The FEBS journal Volume: 276 ISSN: 1742-4658 ISO Abbreviation: FEBS J. Publication Date: 2009 Jan |
Date Detail:
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Created Date: 2009-01-07 Completed Date: 2009-01-29 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 101229646 Medline TA: FEBS J Country: England |
Other Details:
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Languages: eng Pagination: 581-93 Citation Subset: IM |
Affiliation:
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National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Cell Line Chemokines / genetics, metabolism, secretion* Gene Expression Regulation / drug effects, genetics Humans NF-kappa B / metabolism* Ribosome Inactivating Proteins / metabolism Substrate Specificity TNF Receptor-Associated Death Domain Protein / genetics, metabolism TNF Receptor-Associated Factor 2 / genetics, metabolism TNF-Related Apoptosis-Inducing Ligand / pharmacology* p38 Mitogen-Activated Protein Kinases / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Chemokines; 0/NF-kappa B; 0/TNF Receptor-Associated Death Domain Protein; 0/TNF Receptor-Associated Factor 2; 0/TNF-Related Apoptosis-Inducing Ligand; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases; EC 3.2.2.22/Ribosome Inactivating Proteins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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