| Caffeic acid phenethyl ester induces mitochondria-mediated apoptosis in human myeloid leukemia U937 cells. | |
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MedLine Citation:
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PMID: 18060475 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Caffeic acid phenyl ester (CAPE), a biologically active ingredient of propolis, has several interesting biological properties including antioxidant, anti-inflammatory, antiviral, immunostimulatory, anti-angiogenic, anti-invasive, anti-metastatic and carcinostatic activities. Recently, several groups have reported that CAPE is cytotoxic to tumor cells but not to normal cells. In this study, we investigated the mechanism of CAPE-induced apoptosis in human myeloid leukemia U937 cells. Treatment of U937 cells with CAPE decreased cell viability in a dose-dependent and time-dependent manner. DNA fragmentation assay revealed the typical ladder profile of oligonucleosomal fragments in CAPE-treated U937 cells. In addition, as evidenced by the nuclear DAPI staining experiment, we observed that the nuclear condensation, a typical phenotype of apoptosis, was found in U937 cells treated with 5 microg/ml of CAPE. Therefore, it was suggested that CAPE is a potent agent inducing apoptosis in U937 cells. Apoptotic action of the CAPE was accompanied by release of cytochrome C, reduction of Bcl-2 expression, increase of Bax expression, activation/cleavage of caspase-3 and activation/cleavage of PARP in U937 cells, but not by Fas protein, an initial mediator in the death signaling, or by phospho-eIF2 alpha and CHOP, crucial mediators in ER-mediated apoptosis. From the results, it was concluded that CAPE induces the mitochondria-mediated apoptosis but not death receptors- or ER-mediated apoptosis in U937 cells. |
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Authors:
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Un-Ho Jin; Kwon-Ho Song; Muneo Motomura; Ikukatsu Suzuki; Yeun-Hwa Gu; Yun-Jeong Kang; Tae-Chul Moon; Cheorl-Ho Kim |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-11-30 |
Journal Detail:
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Title: Molecular and cellular biochemistry Volume: 310 ISSN: 0300-8177 ISO Abbreviation: Mol. Cell. Biochem. Publication Date: 2008 Mar |
Date Detail:
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Created Date: 2008-02-25 Completed Date: 2008-06-20 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0364456 Medline TA: Mol Cell Biochem Country: Netherlands |
Other Details:
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Languages: eng Pagination: 43-8 Citation Subset: IM |
Affiliation:
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Department of Biological Sciences, Molecular and Cellular Glycobiology Unit, Sungkyunkwan University, 300 Chunchun-Dong, Jangan-Gu, Suwon City, Kyunggi-Do 440-746, Korea. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Antigens, CD95
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metabolism Apoptosis / drug effects* Caffeic Acids / pharmacology* Caspase 3 / metabolism Cell Line, Tumor Chromatin / metabolism Cytochromes c / metabolism DNA Fragmentation / drug effects Endoplasmic Reticulum / drug effects, pathology Eukaryotic Initiation Factor-2 / metabolism Humans Leukemia, Myeloid / pathology* Mitochondria / drug effects*, enzymology, metabolism* Phenylethyl Alcohol / analogs & derivatives*, pharmacology Poly(ADP-ribose) Polymerases / metabolism Proto-Oncogene Proteins c-bcl-2 / metabolism Receptors, Death Domain / metabolism Transcription Factor CHOP / metabolism U937 Cells |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD95; 0/Caffeic Acids; 0/Chromatin; 0/Eukaryotic Initiation Factor-2; 0/FAS protein, human; 0/Proto-Oncogene Proteins c-bcl-2; 0/Receptors, Death Domain; 104594-70-9/caffeic acid phenethyl ester; 147336-12-7/Transcription Factor CHOP; 60-12-8/Phenylethyl Alcohol; 9007-43-6/Cytochromes c; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/Caspase 3 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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