| beta-lapachone induces growth inhibition and apoptosis in bladder cancer cells by modulation of Bcl-2 family and activation of caspases. | |
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MedLine Citation:
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PMID: 16614704 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIM: To study in vitro the molecular mechanism of apoptosis caused by beta-lapachone, a quinone obtained from the bark of the lapacho tree (Tabebuia avellanedae). MATERIALS AND METHODS: The study was carried out on human bladder carcinoma T24 cell line. Determination of cell viability was done using trypan blue exclusion method, apoptosis quantitative estimation - by DAPI staining and agarose gel electrophoresis for DNA fragmentation. Flow cytometry analysis, RT-PCR and Western blot analysis, colorimetric assay of caspase activity were applied as well. RESULTS: It was found that in micromolar range of concentrations beta-lapachone inhibited the viability of T24 cells by inducing apoptosis, which could be proved by formation of apoptotic bodies and DNA fragmentation. Treatment of T24 cells with beta-lapachone resulted in a down-regulation of Bcl-2 expression and up-regulation of Bax expression. beta-lapachone-induced apoptosis was also associated with activation of caspase-3 and caspase-9, inhibition of IAP expression, and degradation of poly (ADP-ribose) polymerase, phospholipase C-gamma1 and beta-catenin proteins. At the same time Fas and FasL levels were inhibited upon treatment with beta-lapachone in a concentration-dependent manner. Conclusion: beta-lapachone-induced apoptosis in T24 cells is mediated, at least in part, by the mitochondrial-signaling pathway. |
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Authors:
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J I Lee; D Y Choi; H S Chung; H G Seo; H J Woo; B T Choi; Y H Choi |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Experimental oncology Volume: 28 ISSN: 1812-9269 ISO Abbreviation: Exp. Oncol. Publication Date: 2006 Mar |
Date Detail:
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Created Date: 2006-04-14 Completed Date: 2006-05-24 Revised Date: 2010-01-15 |
Medline Journal Info:
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Nlm Unique ID: 101230541 Medline TA: Exp Oncol Country: Ukraine |
Other Details:
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Languages: eng Pagination: 30-5 Citation Subset: IM |
Affiliation:
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R&E Program, Korea Science Academy, Busan, South Korea. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antigens, CD95
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metabolism Apoptosis / drug effects* Caspases / metabolism* Cell Division / drug effects* Cell Line, Tumor Cell Survival / drug effects Enzyme Activation / drug effects Fas Ligand Protein Humans Membrane Glycoproteins / metabolism Naphthoquinones / pharmacology* Proto-Oncogene Proteins c-bcl-2 / drug effects, metabolism* RNA, Messenger / drug effects, genetics Reverse Transcriptase Inhibitors / pharmacology Tumor Necrosis Factors / metabolism Urinary Bladder Neoplasms |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD95; 0/FASLG protein, human; 0/Fas Ligand Protein; 0/Membrane Glycoproteins; 0/Naphthoquinones; 0/Proto-Oncogene Proteins c-bcl-2; 0/RNA, Messenger; 0/Reverse Transcriptase Inhibitors; 0/Tumor Necrosis Factors; 4707-32-8/beta-lapachone; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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