| Antitumoral efficacy of four histone deacetylase inhibitors in hepatoma in vitro and in vivo. | |
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MedLine Citation:
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PMID: 23225425 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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BACKGROUND: Histone deacetylase (HDAC) inhibitors are promising antitumoral drugs. Currently there are no data regarding the comparison of different HDAC inhibitors on hepatoma cells. MATERIALS AND METHODS: Hepatoma cells were incubated with the HDAC inhibitors MS-275, SAHA, FK901228 and trichostatin. Proliferation was assessed via BrdU incorporation and apoptosis rate via flow cytometry. Trichostatin, SAHA and MS-275 were applied in a rat hepatoma model. RESULTS: The agents showed antiproliferative and pro-apoptotic effects time- and dose-dependently. SAHA and MS-275 were moderately effective at 10 μM, while trichostatin A and FK901228 showed higher potency. Caspases 3 and 8 were activated upon treatment with the drugs. The agents increased the acetylation rate. Hyperacetylation did not correlate with antitumoral efficacy. In vivo, SAHA was superior to MS-275 and trichostatin A. CONCLUSION: The HDAC inhibitors were effective both in vitro and in vivo. The potency of SAHA and MS-275 was similar. In spite of differing affinity to the 11 known HDACs, the agents induced comparable effects. These findings suggest that these agents have further antitumoral effects apart from HDAC inhibition. |
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Authors:
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Marion Ganslmayer; Peter Konturek; Christoph Herold; Markus F Neurath; Steffen Zopf |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Anticancer research Volume: 32 ISSN: 1791-7530 ISO Abbreviation: Anticancer Res. Publication Date: 2012 Dec |
Date Detail:
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Created Date: 2012-12-10 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8102988 Medline TA: Anticancer Res Country: Greece |
Other Details:
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Languages: eng Pagination: 5263-9 Citation Subset: IM |
Affiliation:
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Department of Medicine I, University hospital Erlangen, Ulmenweg 18, D-91054 Erlangen, Germany. marion.ganslmayer@uk-erlangen.de. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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