Please use this identifier to cite or link to this item:https://hdl.handle.net/20.500.12259/34251
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dc.contributor.authorKubiliūtė, Raimonda-
dc.contributor.authorŠulskytė, Indrė-
dc.contributor.authorDaniūnaitė, Kristina-
dc.contributor.authorDaugelavičius, Rimantas-
dc.contributor.authorJarmalaitė, Sonata-
dc.coverage.spatialLT-
dc.date.accessioned2017-04-04T07:15:00Z-
dc.date.available2017-04-04T07:15:00Z-
dc.date.issued2016-
dc.identifier.issn1010660X-
dc.identifier.otherVDU02-000020260-
dc.identifier.urihttps://doi.org/10.1016/j.medici.2016.09.003-
dc.identifier.urihttps://eltalpykla.vdu.lt/1/34251-
dc.descriptioneISSN 1648-9144-
dc.description.abstractBackground and aim: Resistance to chemotherapy is the key obstacle to the effective treatment of various cancers. Accumulating evidence suggests significant involvement of the epithelial-to-mesenchymal transition (EMT) in the chemoresistance of most cancer types. This study aimed at analyzing the gene expression profile of doxorubicin (DOX)-resistant colorectal cancer cells CX-1. Materials and methods: DOX-resistant CX-1 cell sublines were acquired by stepwise increment of DOX concentrations in cell growth media. Global gene expression profiling was performed using human gene expression microarrays. The expression levels of individual genes were assessed by means of quantitative PCR (qPCR), while the DNA methylation pattern of several selected genes was determined by methylation-specific PCR. Results: Four DOX-resistant CX-1 sublines were established as a valuable tool for cell chemoresistance studies. Altered expression of the EMT, cell adhesion and motility, and chemoresistance-related genes was observed in DOX-resistant cells by genome-wide gene expression analysis. Besides, early and significant upregulation of the key EMT genes ZEB1 (5.8 ; P < 0.001) and CDH2 (6.2 ; P = 0.044) was identified by qPCR, with subsequent activation of drug transporter gene ABCC1 (3.3 ; P = 0.007) and cell stemness gene NANOG (2.4 ; P = 0.008). Downregulation of TET1 (2.1 ; P = 0.041) and changes in the methylation status of the p16 gene were also involved in the acquisition of cell resistance to DOXen
dc.description.sponsorshipBiochemijos katedra-
dc.description.sponsorshipGamtos mokslų fakultetas-
dc.description.sponsorshipNacionalinis vėžio institutas-
dc.description.sponsorshipVilniaus universitetas-
dc.description.sponsorshipVytauto Didžiojo universitetas-
dc.format.extentp. 298-306-
dc.language.isoen-
dc.relation.ispartofMedicina. Kaunas : Lietuvos sveikatos mokslų universitetas, 2016, T. 52, nr. 5-
dc.relation.isreferencedbyScience Citation Index Expanded (Web of Science)-
dc.relation.isreferencedbyMEDLINE-
dc.relation.isreferencedbyScopus-
dc.relation.isreferencedbyIndexCopernicus-
dc.relation.isreferencedbyScienceDirect-
dc.rightsSutarties data 2016-12-20, nr. B000196, laisvai prieinamas internetelt_LT
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.subjectŽarnyno vėžyslt
dc.subjectCX-1 ląstelėslt
dc.subjectAtsparumas doksorubicinuilt
dc.subjectEpitelinis-mezenchiminis virsmaslt
dc.subjectColon cancer CX-1en
dc.subjectDoxorubicin resistanceen
dc.subjectEpithelial-to-mesenchymal transitionen
dc.subject.otherBiochemija / Biochemistry (N004)-
dc.subject.otherBiologija / Biology (N010)-
dc.titleMolecular features of doxorubicin-resistance development in colorectal cancer CX-1 cell lineen
dc.typeStraipsnis Clarivate Analytics Web of Science ar/ir Scopus / Article in Clarivate Analytics Web of Science or / and Scopus (S1)-
dc.identifier.doihttps://doi.org/10.1016/j.medici.2016.09.003-
dc.identifier.isiWOS:000388594700006-
dcterms.bibliographicCitation34-
dc.date.updated2020-02-07T14:31Z-
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local.typeS-
item.fulltextWith Fulltext-
item.grantfulltextopen-
crisitem.author.deptBiochemijos katedra-
crisitem.author.deptBiochemijos katedra-
crisitem.author.deptFizikos katedra-
crisitem.author.deptBiochemijos katedra-
crisitem.author.deptVytauto Didžiojo universitetas-
Appears in Collections:1. Straipsniai / Articles
Universiteto mokslo publikacijos / University Research Publications
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