DC Field | Value | Language |
---|---|---|
dc.contributor.author | Noh, Eun Loo | ko |
dc.contributor.author | Lim, Dae-Sik | ko |
dc.contributor.author | Jeong, Gajin | ko |
dc.contributor.author | Lee, Jong-Soo | ko |
dc.date.accessioned | 2013-03-09T21:04:10Z | - |
dc.date.available | 2013-03-09T21:04:10Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2009-01 | - |
dc.identifier.citation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.378, no.3, pp.326 - 331 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | http://hdl.handle.net/10203/97454 | - |
dc.description.abstract | Histone deacetylases (HDACs), a promising target for cancer therapy, play a role in regulating cell-cycle progression. The mechanisms for HDAC inhibition-induced regulation of G(2)/M transition and mitotic progression remain to be elucidated. Herein, we report that trichostatin A (TSA), an HDAC inhibitor, induces a delay at the G(2)/M transition, chromosome missegregation and multi-nucleation. and thereby leads to cell death by promoting exit from aberrant mitosis without spindle checkpoint. These results are associated with a transcriptional modulation of key regulator genes of the cell cycle, including CyclinB1, PIk1, Survivin, and P21(WAF1/Cip1). Actinomycin D, a transcriptional inhibitor, abrogated the TSA-induced delay of G(2)/M transition and transcriptional modulation of cell-cycle regulator genes, indicating that the impact of TSA in this manner is transcription dependent. Overall, our findings indicate that TSA provides a barrier to cell-cycle progression for antiproliferation and promotes escape from mitotic catastrophe and cell death, by inhibiting an HDAC-mediated transcriptional action. (C) 2008 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.subject | HISTONE DEACETYLASE INHIBITORS | - |
dc.subject | CANCER CELLS | - |
dc.subject | CYTOTOXICITY | - |
dc.subject | PATHWAY | - |
dc.title | An HDAC inhibitor, trichostatin A, induces a delay at G(2)/M transition, slippage of spindle checkpoint, and cell death in a transcription-dependent manner | - |
dc.type | Article | - |
dc.identifier.wosid | 000262343200002 | - |
dc.identifier.scopusid | 2-s2.0-57749189353 | - |
dc.type.rims | ART | - |
dc.citation.volume | 378 | - |
dc.citation.issue | 3 | - |
dc.citation.beginningpage | 326 | - |
dc.citation.endingpage | 331 | - |
dc.citation.publicationname | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.identifier.doi | 10.1016/j.bbrc.2008.11.057 | - |
dc.embargo.liftdate | 9999-12-31 | - |
dc.embargo.terms | 9999-12-31 | - |
dc.contributor.localauthor | Lim, Dae-Sik | - |
dc.contributor.nonIdAuthor | Noh, Eun Loo | - |
dc.contributor.nonIdAuthor | Jeong, Gajin | - |
dc.contributor.nonIdAuthor | Lee, Jong-Soo | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | Histone deacetylase | - |
dc.subject.keywordAuthor | Trichostatin A | - |
dc.subject.keywordAuthor | Transcription | - |
dc.subject.keywordAuthor | Cell cycle | - |
dc.subject.keywordAuthor | Cell death | - |
dc.subject.keywordPlus | HISTONE DEACETYLASE INHIBITORS | - |
dc.subject.keywordPlus | CANCER CELLS | - |
dc.subject.keywordPlus | CYTOTOXICITY | - |
dc.subject.keywordPlus | PATHWAY | - |
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