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dc.contributor.authorPan, Chun-Haoen_US
dc.contributor.authorChang, Ying-Fangen_US
dc.contributor.authorLee, Ming-Shuoen_US
dc.contributor.authorWen, B-Chenen_US
dc.contributor.authorKo, Jen-Chungen_US
dc.contributor.authorLiang, Sheng-Kaien_US
dc.contributor.authorLiang, Mei-Chihen_US
dc.date.accessioned2019-04-03T06:37:15Z-
dc.date.available2019-04-03T06:37:15Z-
dc.date.issued2016-11-07en_US
dc.identifier.issn1471-2407en_US
dc.identifier.urihttp://dx.doi.org/10.1186/s12885-016-2888-7en_US
dc.identifier.urihttp://hdl.handle.net/11536/132821-
dc.description.abstractBackground: Vorinostat, a histone deacetylase (HDAC) inhibitor, is a promising agent for cancer therapy. Combining vorinostat with cisplatin may relax the chromatin structure and facilitate the accessibility of cisplatin, thus enhancing its cytotoxicity. Studies have not yet investigated the effects of the combination of vorinostat and cisplatin on small cell lung cancer (SCLC). Methods: We first assessed the efficacy of vorinostat with etoposide/cisplatin (EP; triple combination) and then investigated the effects of cotreatment with vorinostat and cisplatin on H209 and H146 SCLC cell lines. The anticancer effects of various combinations were determined in terms of cell viability, apoptosis, cell cycle distribution, and vorinostat-regulated proteins. We also evaluated the efficacy of vorinostat/cisplatin combination in H209 xenograft nude mice. Results: Our data revealed that the triple combination engendered a significant reduction of cell viability and high apoptotic cell death. In addition, vorinostat combined with cisplatin enhanced cell growth inhibition, induced apoptosis, and promoted cell cycle arrest. We observed that the acetylation levels of histone H3 and a-tubulin were higher in combination treatments than in vorinostat treatment alone. Moreover, vorinostat reduced the expression of thymidylate synthase (TS), and TS remained inhibited after cotreament with cisplatin. Furthermore, an in vivo study revealed that the combination of vorinostat and cisplatin significantly inhibited tumor growth in xenograft nude mice (tumor growth inhibition T/C% = 20.5 %). Conclusions: Combined treatments with vorinostat promote the cytotoxicity of cisplatin and induce the expression of vorinostat-regulated acetyl proteins, eventually enhancing antitumor effects in SCLC cell lines. Triple combinations with a low dosage of cisplatin demonstrate similar therapeutic effects. Such triple combinations, if applied clinically, may reduce the undesired adverse effects of cisplatin. The effects of the combination of vorinostat and cisplatin should be evaluated further before conducting clinical trials for SCLC treatment.en_US
dc.language.isoen_USen_US
dc.subjectVorinostaten_US
dc.subjectCisplatinen_US
dc.subjectSCLCen_US
dc.subjectHDAC inhibitoren_US
dc.subjectCombination therapyen_US
dc.titleVorinostat enhances the cisplatin-mediated anticancer effects in small cell lung cancer cellsen_US
dc.typeArticleen_US
dc.identifier.doi10.1186/s12885-016-2888-7en_US
dc.identifier.journalBMC CANCERen_US
dc.citation.volume16en_US
dc.citation.spage0en_US
dc.citation.epage0en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.department分子醫學與生物工程研究所zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.contributor.departmentInstitute of Molecular Medicine and Bioengineeringen_US
dc.identifier.wosnumberWOS:000387640200001en_US
dc.citation.woscount7en_US
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