| Acetyl-keto-beta-boswellic acid induces apoptosis through a death receptor 5-mediated pathway in prostate cancer cells. | |
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MedLine Citation:
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PMID: 18281494 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Acetyl-keto-beta-boswellic acid (AKBA), a triterpenoid isolated from Boswellia carterri Birdw and Boswellia serrata, has been found to inhibit tumor cell growth and to induce apoptosis. The apoptotic effects and the mechanisms of action of AKBA were studied in LNCaP and PC-3 human prostate cancer cells. AKBA induced apoptosis in both cell lines at concentrations above 10 microg/mL. AKBA-induced apoptosis was correlated with the activation of caspase-3 and caspase-8 as well as with poly(ADP)ribose polymerase (PARP) cleavage. The activation of caspase-8 was correlated with increased levels of death receptor (DR) 5 but not of Fas or DR4. AKBA-induced apoptosis, caspase-8 activation, and PARP cleavage were inhibited by knocking down DR5 using a small hairpin RNA. AKBA treatment increased the levels of CAAT/enhancer binding protein homologous protein (CHOP) and activated a DR5 promoter reporter but did not activate a DR5 promoter reporter with the mutant CHOP binding site. These results suggest that AKBA induces apoptosis in prostate cancer cells through a DR5-mediated pathway, which probably involves the induced expression of CHOP. |
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Authors:
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Min Lu; Lijuan Xia; Huiming Hua; Yongkui Jing |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Cancer research Volume: 68 ISSN: 1538-7445 ISO Abbreviation: Cancer Res. Publication Date: 2008 Feb |
Date Detail:
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Created Date: 2008-02-18 Completed Date: 2008-03-11 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 2984705R Medline TA: Cancer Res Country: United States |
Other Details:
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Languages: eng Pagination: 1180-6 Citation Subset: IM |
Affiliation:
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Division of Hematology/Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029-6547, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis
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drug effects* Binding Sites CCAAT-Enhancer-Binding Proteins / biosynthesis, metabolism Caspase 3 / metabolism Caspase 8 / metabolism Cell Growth Processes / drug effects Cell Line, Tumor Enzyme Activation Humans Male Neoplasms, Hormone-Dependent / drug therapy*, genetics, metabolism, pathology Promoter Regions, Genetic Prostatic Neoplasms / drug therapy*, genetics, metabolism, pathology RNA, Messenger / biosynthesis, genetics RNA, Small Interfering / genetics Receptors, TNF-Related Apoptosis-Inducing Ligand / biosynthesis, genetics, metabolism* TNF-Related Apoptosis-Inducing Ligand / metabolism Triterpenes / pharmacology* Up-Regulation |
| Grant Support | |
ID/Acronym/Agency:
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R21AT001539/AT/NCCAM NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/CCAAT-Enhancer-Binding Proteins; 0/RNA, Messenger; 0/RNA, Small Interfering; 0/Receptors, TNF-Related Apoptosis-Inducing Ligand; 0/TNF-Related Apoptosis-Inducing Ligand; 0/TNFSF10 protein, human; 0/Triterpenes; 0/acetyl-11-ketoboswellic acid; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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