Publication:
Splicing variants of versican in CD133+/CD44+ prostate cancer stem cells

dc.contributor.coauthorAyla, Sule
dc.contributor.coauthorKarakoc, Emre
dc.contributor.coauthorByrne, Yasemin Yozgat
dc.contributor.coauthorParlayan, Cuneyd
dc.contributor.coauthorKeskin, Ilknur
dc.contributor.coauthorTaskiran, Aysegul
dc.contributor.coauthorOktem, Gulperi
dc.contributor.kuauthorKarahüseyinoğlu, Serçin
dc.contributor.researchcenter 
dc.contributor.schoolcollegeinstituteSchool of Medicine
dc.contributor.unit 
dc.date.accessioned2024-12-29T09:39:17Z
dc.date.issued2024
dc.description.abstractA cancer mass is composed of a heterogeneous group of cells, a small part of which constitutes the cancer stem cells since they are less differentiated and have a high capacity to develop cancer. Versican is an extracellular matrix protein located in many human tissues. The mRNA of versican has been shown to have "splicing patterns" as detected by RT-PCR, northern blot analysis, and cDNA sequencing. Based on this knowledge this study aims to reveal the splice variants of versican molecules, which are thought to be involved in the pathogenesis of the DU145 human prostatic carcinoma cell line and prostatic cancer stem cells isolated from this cell line. In this study, RWPE-1 normal prostatic and DU-145 human prostate cancer cell lines have been used. Prostatic cancer stem cells and the remaining group of non-prostatic-cancer stem cells (bulk population) were isolated according to their CD133+/CD44+. RNA was isolated in all groups, and sequence analysis was accomplished for splicing variants by Illumina NextSeq 500 sequencing system. The results were analyzed by bioinformatic evaluation. As five isoforms of the versican gene in the differential transcript expression are analyzed, it was observed that a significant change was only found in the isoforms Versican 0 and Versican 1. In this study, we explored the function of this molecule which we think to be effective in cancer progression, and suggested that more valuable results can be obtained after the accomplishment of in vivo experiments.
dc.description.indexedbyWoS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.openaccess 
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuTÜBİTAK
dc.description.sponsorsThis project was supported by the Scientific and Technological Research Council of Turkey (TUBITAK 3001 ARDEB Program-grant number 116S150).r Research Council of Turkey (TUBITAK 3001 ARDEB Program-grant number 116S150) .
dc.description.volume260
dc.identifier.doi10.1016/j.prp.2024.155440
dc.identifier.eissn1618-0631
dc.identifier.issn0344-0338
dc.identifier.link 
dc.identifier.quartileQ2
dc.identifier.scopus2-s2.0-85197408368
dc.identifier.urihttps://doi.org/10.1016/j.prp.2024.155440
dc.identifier.urihttps://hdl.handle.net/20.500.14288/22968
dc.identifier.wos1265418700001
dc.keywordsProstate cancer
dc.keywordsCancer stem cell
dc.keywordsVersican
dc.keywordsAdhesion molecule
dc.languageen
dc.publisherElsevier GMBH
dc.relation.grantno 
dc.rights 
dc.sourcePathology Research and Practice
dc.subjectPathology
dc.titleSplicing variants of versican in CD133+/CD44+ prostate cancer stem cells
dc.typeJournal article
dc.type.other 
dspace.entity.typePublication
local.contributor.kuauthorKarahüseyinoğlu, Serçin

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