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dc.contributor.authorAyla, Şule
dc.contributor.authorKarakoç, Emre
dc.contributor.authorYozgat Byrne, Yasemin
dc.contributor.authorParlayan, Cüneyd
dc.contributor.authorKeskin, İlknur
dc.contributor.authorKarahüseyinoğlu, Serçin
dc.contributor.authorTaşkıran, Ayşegül
dc.contributor.authorÖktem, Gülperi
dc.date.accessioned2024-07-11T06:11:53Z
dc.date.available2024-07-11T06:11:53Z
dc.date.issued2024en_US
dc.identifier.citationAyla, Ş., Karakoç, E., Yozgat Byrne, Y., Parlayan, C., Keskin, İ., Karahüseyinoğlu, S. ... Öktem, G. (2024). Splicing variants of versican in CD133+/CD44+ prostate cancer stem cells. Pathology Research and Practice, 260. http://dx.doi.org/10.1016/j.prp.2024.155440en_US
dc.identifier.issn0344-0338
dc.identifier.issn1618-0631
dc.identifier.urihttp://dx.doi.org/10.1016/j.prp.2024.155440
dc.identifier.urihttps://hdl.handle.net/20.500.12511/12710
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 DU-145 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.en_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAdhesion Moleculeen_US
dc.subjectCancer Stem Cellen_US
dc.subjectProstate Canceren_US
dc.subjectVersicanen_US
dc.titleSplicing variants of versican in CD133+/CD44+ prostate cancer stem cellsen_US
dc.typearticleen_US
dc.relation.ispartofPathology Research and Practiceen_US
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Sağlık Bilim ve Teknolojileri Araştırma Enstitüsüen_US
dc.departmentİstanbul Medipol Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Histoloji ve Embriyoloji Ana Bilim Dalıen_US
dc.authorid0000-0003-1580-8371en_US
dc.authorid0000-0002-7059-1884en_US
dc.identifier.volume260en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1016/j.prp.2024.155440en_US
dc.institutionauthorYozgat Byrne, Yasemin
dc.institutionauthorKeskin, İlknur
dc.identifier.wosqualityQ2en_US
dc.identifier.wos001265418700001en_US
dc.identifier.scopus2-s2.0-85197408368en_US
dc.identifier.pmid38964119en_US
dc.identifier.scopusqualityQ2en_US


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