Tunicamycin-induced endoplasmic reticulum stress reduces in vitro subpopulation and invasion of CD44+/CD24-phenotype breast cancer stem cells

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dc.contributor.authorNami, Babak
dc.contributor.authorDonmez, Huseyin
dc.contributor.authorKocak, Nadir
dc.date.accessioned2020-03-26T19:31:47Z
dc.date.available2020-03-26T19:31:47Z
dc.date.issued2016
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractTunicamycin is an inhibitor of glycosylation that disturbs protein folding machinery in eukaryotic cells. Tunicamycin causes accumulation of unfolded proteins in cell endoplasmic reticulum (ER) and induces ER stress. ER stress is an essential mechanism for cellular homeostasis has role in cell death via reprogramming of protein processing, regulation of autophagy and apoptosis. In this study we show effect of tunicamycin on subpopulation and invasion of CD44+/CD24- MCF7 breast cancer stem cells. CD44+/CD24- cells were isolated from MCF7 cell line by fluorescence activated cell sorting (FACS) and treated with tunicamycin. ER stress was monitored by evaluation of X-box binding protein 1(XBP-1) mRNA splicing, cleaved activating transcription factor 6 (ATF6) nuclear translocation and CCAAT/enhancer-binding protein homologous protein (CHOP) expression. CD44+/CD24- subpopulation was analyzed using flow cytometry. Invasion was investigated by scratch assay, trypan blue staining, 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide (MTT) proliferation and in vitro migration assays. Increased level of spliced XBP-1, ATF6 nuclear translocation and CHOP protein expression were detected in CD44+/CD24- and original MCF7 cells treated with tunicamycin. Also, a significant decline in CD44+/CD24- cell subpopulation was determined in the cells treated with tunicamycin. The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin. Our results indicate that CD44+/CD24- phenotype MCF7 cells are susceptible to tunicamycin. The results showed that tunicamycin-induced ER stress suppresses CD44+/CD24- phenotype cell subpopulation and in vitro invasion and accelerates tumorosphore formation. These results suggest that tunicamycin-induced ER stress inhibits CD44+/CD24- phenotype MCF7 breast cancer stem cells. We conclude that using ER-targeting chemicals like tunicamycin is an interesting approach to target breast cancer stem cells inside tumor. (C) 2016 Elsevier GmbH. All rights reserved.en_US
dc.identifier.doi10.1016/j.etp.2016.06.004en_US
dc.identifier.endpage426en_US
dc.identifier.issn0940-2993en_US
dc.identifier.issn1618-1433en_US
dc.identifier.issue7en_US
dc.identifier.pmid27350212en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage419en_US
dc.identifier.urihttps://dx.doi.org/10.1016/j.etp.2016.06.004
dc.identifier.urihttps://hdl.handle.net/20.500.12395/34164
dc.identifier.volume68en_US
dc.identifier.wosWOS:000381652700006en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherELSEVIER GMBHen_US
dc.relation.ispartofEXPERIMENTAL AND TOXICOLOGIC PATHOLOGYen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectTunicamycinen_US
dc.subjectEndoplasmic reticulum stressen_US
dc.subjectBreast canceren_US
dc.subjectCancer stem cellsen_US
dc.subjectCD44en_US
dc.subjectCD24en_US
dc.titleTunicamycin-induced endoplasmic reticulum stress reduces in vitro subpopulation and invasion of CD44+/CD24-phenotype breast cancer stem cellsen_US
dc.typeArticleen_US

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