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

dc.authorid0000-0001-5531-2587
dc.authorid0000-0001-9780-6948
dc.authorid0000-0002-2324-8127
dc.contributor.authorAyla, Sule
dc.contributor.authorKarakoc, Emre
dc.contributor.authorByrne, Yasemin Yozgat
dc.contributor.authorParlayan, Cuneyd
dc.contributor.authorKeskin, Ilknur
dc.contributor.authorKarahuseyinoglu, Sercin
dc.contributor.authorTaskiran, Aysegul
dc.date.accessioned2025-05-10T19:43:27Z
dc.date.issued2024
dc.departmentİstanbul Medeniyet Üniversitesi
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.sponsorshipResearch Council of Turkey (TUBITAK 3001 ARDEB Program-grant) [116S150]
dc.description.sponsorshipThis 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.identifier.doi10.1016/j.prp.2024.155440
dc.identifier.issn0344-0338
dc.identifier.issn1618-0631
dc.identifier.pmid38964119
dc.identifier.scopus2-s2.0-85197408368
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1016/j.prp.2024.155440
dc.identifier.urihttps://hdl.handle.net/20.500.14730/10605
dc.identifier.volume260
dc.identifier.wosWOS:001265418700001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Gmbh
dc.relation.ispartofPathology Research and Practice
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250302
dc.subjectProstate cancer
dc.subjectcancer stem cell
dc.subjectversican
dc.subjectadhesion molecule
dc.titleSplicing variants of versican in CD133+/CD44+prostate cancer stem cells
dc.typeArticle

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