| Caffeic acid phenethyl ester induces growth arrest and apoptosis of colon cancer cells via the beta-catenin/T-cell factor signaling. | |
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MedLine Citation:
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PMID: 16926625 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Caffeic acid phenethyl ester, an active component of propolis, has been implicated in the regulation of cell growth and apoptosis, although the exact mechanism of this activity has not been elucidated. In this study, we explored the effects of caffeic acid phenethyl ester on growth, cell cycle, apoptosis and beta-catenin/T-cell factor signaling in human colon cancer cells. Using two human sporadic colon cancer cell lines (HCT116 and SW480), we assayed for cell growth inhibition, cell cycle and apoptosis induction. We also assayed for beta-catenin and downstream target genes (cyclin D1 and c-myc) mRNA and protein expression by reverse transcriptase-polymerase chain reaction and Western blot analysis. Beta-catenin localization was detected by indirect immunofluorescence. Beta-catenin/T-cell factor transcriptional activity was determined by transient transfection and reporter gene assay. Caffeic acid phenethyl ester completely inhibited growth, and induced G1 phase arrest and apoptosis in a dose-dependent manner in both HCT116 and SW480 cells. Treatment of human colon cancer cells with apoptotic concentrations of caffeic acid phenethyl ester resulted in a dose-dependent and time-dependent loss of total beta-Catenin protein, associated with decreased nuclear beta-catenin. Caffeic acid phenethyl ester reduced the expression of cyclin D1 and c-myc in a dose-dependent and time-dependent manner. We proved that caffeic acid phenethyl ester markedly suppressed the transcriptional activity of beta-catenin/T-cell factor in both HCT116 and SW480 cells depending on the concentration of caffeic acid phenethyl ester. These results indicate that caffeic acid phenethyl ester is an excellent inhibitor of beta-catenin/T-cell factor signaling in colon cancer cell lines and suggest that caffeic acid phenethyl ester merits further study as an agent against colorectal cancers. |
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Authors:
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Debing Xiang; Dong Wang; Yujun He; Jiayin Xie; Zhaoyang Zhong; Zengpeng Li; Jiang Xie |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Anti-cancer drugs Volume: 17 ISSN: 0959-4973 ISO Abbreviation: Anticancer Drugs Publication Date: 2006 Aug |
Date Detail:
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Created Date: 2006-08-23 Completed Date: 2006-12-12 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9100823 Medline TA: Anticancer Drugs Country: England |
Other Details:
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Languages: eng Pagination: 753-62 Citation Subset: IM |
Affiliation:
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Cancer Center, Daping Hospital and Institute of Surgery, Third Military Medical University, Chongqing, PRC. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Annexin A5
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metabolism Apoptosis / drug effects* Blotting, Western Caffeic Acids / pharmacology* Cell Cycle / drug effects Cell Division / drug effects Cell Line, Tumor Colonic Neoplasms / drug therapy*, pathology* Cyclin D1 / genetics Flow Cytometry Fluorescent Antibody Technique, Indirect Genes, Reporter / genetics Genes, myc / genetics Humans Phenylethyl Alcohol / analogs & derivatives*, pharmacology Reverse Transcriptase Polymerase Chain Reaction Signal Transduction / drug effects* Transfection beta Catenin / genetics, metabolism, physiology* |
| Chemical | |
Reg. No./Substance:
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0/Annexin A5; 0/Caffeic Acids; 0/beta Catenin; 104594-70-9/caffeic acid phenethyl ester; 136601-57-5/Cyclin D1; 60-12-8/Phenylethyl Alcohol |
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