HDAC inhibitors, MS-275 and salermide, potentiates the anticancer effect of EF24 in human pancreatic cancer cells

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dc.contributor.authorYar Sağlam, Atiye Seda
dc.contributor.authorYılmaz, Akın
dc.contributor.authorÖnen, İlke Hacer
dc.contributor.authorAlp, Ebru
dc.contributor.authorKayhan, Handan
dc.contributor.authorEkmekci, Abdullah
dc.date.accessioned2019-05-13T09:06:52Z
dc.date.available2019-05-13T09:06:52Z
dc.date.issued2016
dc.departmentHitit Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü
dc.description.abstractHistone deacetylases (HDACs) play a major role in the regulation of chromatin structure and gene expression by changing acetylation status of histone and non-histone proteins. MS-275 (entinostat, MS) is a well-known benzamide- based HDACI and Salermide (SAL), a reverse amide compound HDACI, have antiproliferative effects on several human cancer cells. In this study, we aimed to investigate the effects of HDACIs (MS and SAL) alone and/or combined use with EF24 (EF), a novel synthetic curcumin analog, on human pancreatic cancer cell line (BxPC-3). In vitro, BxPC-3 cells were exposed to varying concentrations of MS, SAL with or without EF, and their effects on cell viability, acetylated Histone H3 and H4 levels, cytotoxicity, and cleaved caspase 3 levels, and cell cycle distribution were measured. The viability of BxPC-3 cells decreased significantly after treatment with EF, MS and SAL treatments. MS and SAL treatment increased the acetylation of histone H3 and H4 in a dose dependent manner. MS and SAL alone or combined with EF were increased the number of cells in G1 phase. In addition, treatment with agents significantly decreased the ratio of cell in G2/M phase. There were significant dose-dependent increases at cleaved Caspase 3 levels after MS treatment but not after SAL treatment. Our results showed that HDAC inhibitors (MS and SAL), when combined with EF, may effectively reduce pancreatic cancer cell (BxPC-3) progression and stop the cell cycle at G1 phase. Further molecular analyses are needed to understand the fundamental molecular consequences of HDAC inhibition in pancreas cancer cells. © 2016, Leibniz Research Centre for Working Environment and Human Factors. All rights reserved.
dc.identifier.citationYar Sağlam, A. S., Yılmaz, A., Önen, H. İ., Alp, E., Kayhan, H., Ekmekci, A. (2016). HDAC inhibitors, MS-275 and salermide, potentiates the anticancer effect of EF24 in human pancreatic cancer cells. EXCLI Journal, 15, 246-255.
dc.identifier.doi10.17179/excli2016-186
dc.identifier.endpage255en_US
dc.identifier.issn1611-2156
dc.identifier.scopusqualityQ1
dc.identifier.startpage246en_US
dc.identifier.urihttps://doi.org/10.17179/excli2016-186
dc.identifier.urihttps://hdl.handle.net/11491/1670
dc.identifier.volume15en_US
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherLeibniz Research Centre for Working Environment and Human Factors
dc.relation.ispartofEXCLI Journal
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectBxpc-3 Cellsen_US
dc.subjectEF24en_US
dc.subjectHDACIen_US
dc.subjectMS-275en_US
dc.subjectPancreatic Canceren_US
dc.subjectSalermideen_US
dc.titleHDAC inhibitors, MS-275 and salermide, potentiates the anticancer effect of EF24 in human pancreatic cancer cells
dc.typeArticle

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