Two different docetaxel resistant MCF-7 sublines exhibited different gene expression pattern

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dc.contributor.authorİşeri O.D.
dc.contributor.authorKars M.D.
dc.contributor.authorGündüz U.
dc.date.accessioned2020-03-26T18:33:03Z
dc.date.available2020-03-26T18:33:03Z
dc.date.issued2012
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractThe objective of the present study was to investigate gene expression pattern of two docetaxel resistant MCF-7 breast carcinoma sublines step wisely selected in 30 and 120 nM docetaxel. Cell proliferation assay was performed in order to demonstrate development of docetaxel resistance. cDNA microarray analysis was performed using Affymetrix® Human Genome U133 Plus 2.0 Arrays in duplicate experiments. Quantitative and semi-quantitative gene expression analysis was also performed to confirm gene expression analysis for selected genes. XTT results demonstrated that 30 (MCF-7/30nM DOC) and 120 nM (MCF-7/120nM DOC) docetaxel selected cells were 13-and 47-fold resistant, respectively. cDNA microarray analysis demonstrated that expression profiles of MCF-7 and MCF-7/30nM DOC were more similar to each other where expression profile of MCF-7/ 120nM DOC was different as examined by line graphs and scatter plots. 2,837 and 4,036 genes were significantly altered in 30 and 120 nM docetaxel resistant sublines, respectively. Among these, 849 genes were altered in common in two docetaxel resistant sublines. Antiapoptotic gene expression (e.g., Bcl-2 and APRIL) were noticeably altered in MCF-7/30nM DOC. However, docetaxel resistance in MCF-7/120nM DOC were more complicated with the involvement of ECM related gene expression, cytokine and growth factor signaling, ROS metabolism and EMT related gene expression together with higher level of MDR1 expression. Expression profiles in 30 and 120 nM docetaxel resistant sublines changed gradually with increasing resistance index. Drug resistance development seems to be step wise event in MCF-7 cells. © Springer Science+Business Media B.V. 2011.en_US
dc.description.sponsorshipSBAG 3297 Türkiye Bilimsel ve Teknolojik Araştirma Kurumuen_US
dc.description.sponsorshipAcknowledgments We gratefully acknowledge Prof. Dr. Fikret Arpacı and Prof. Dr. Ali Ug?ur Ural (Gülhane Military School of Medicine). This study was supported by The Scientific and Technological Research Council of Turkey (TUBITAK; SBAG 3297).en_US
dc.identifier.doi10.1007/s11033-011-1123-5en_US
dc.identifier.endpage3516en_US
dc.identifier.issn0301-4851en_US
dc.identifier.issue4en_US
dc.identifier.pmid21720762en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage3505en_US
dc.identifier.urihttps://dx.doi.org/10.1007/s11033-011-1123-5
dc.identifier.urihttps://hdl.handle.net/20.500.12395/28829
dc.identifier.volume39en_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherKluwer Academic Publishersen_US
dc.relation.ispartofMolecular Biology Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectCDNA microarrayen_US
dc.subjectDocetaxelen_US
dc.subjectMCF-7en_US
dc.subjectMultidrug resistanceen_US
dc.titleTwo different docetaxel resistant MCF-7 sublines exhibited different gene expression patternen_US
dc.typeArticleen_US

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