Upregulated Wnt-11 and miR-21 Expression Trigger Epithelial Mesenchymal Transition in Aggressive Prostate Cancer Cells

dc.contributor.authorArisan, Elif Damla
dc.contributor.authorRencuzogullari, Ozge
dc.contributor.authorFreitas, Ines Lua
dc.contributor.authorRadzali, Syanas
dc.contributor.authorKeskin, Buse
dc.contributor.authorKothari, Archana
dc.contributor.authorWarford, Antony
dc.date.accessioned2025-10-29T11:09:07Z
dc.date.issued2020
dc.departmentEnstitüler, Lisansüstü Eğitim Enstitüsü, Biyomühendislik Ana Bilim Dalı
dc.description.abstractProstate cancer (PCa) is the second-leading cause of cancer-related death among men. microRNAs have been identified as having potential roles in tumorigenesis. An oncomir, miR-21, is commonly highly upregulated in many cancers, including PCa, and showed correlation with the Wnt-signaling axis to increase invasion. Wnt-11 is a developmentally regulated gene and has been found to be upregulated in PCa, but its mechanism is unknown. The present study aimed to investigate the roles of miR-21 and Wnt-11 in PCa in vivo and in vitro. First, different Gleason score PCa tissue samples were used; both miR-21 and Wnt-11 expressions correlate with high Gleason scores in PCa patient tissues. This data then was confirmed with formalin-fixed paraffin cell blocks using PCa cell lines LNCaP and PC3. Cell survival and colony formation studies proved that miR-21 involves in cells' behaviors, as well as the epithelial-mesenchymal transition. Consistent with the previous data, silencing miR-21 led to significant inhibition of cellular invasiveness. Overall, these results suggest that miR-21 plays a significant role related to Wnt-11 in the pathophysiology of PCa.
dc.description.sponsorshipStart up Fund
dc.description.sponsorshipThis study was part funded by Start up Fund to P Uysal-Onganer by the University ofWestminster.
dc.identifier.doi10.3390/biology9030052
dc.identifier.issn2079-7737
dc.identifier.issue3
dc.identifier.orcid0000-0003-3190-8831
dc.identifier.orcid0000-0002-2157-1289
dc.identifier.orcid0000-0002-9756-3330
dc.identifier.orcid0000-0002-4844-6381
dc.identifier.pmid32182839
dc.identifier.scopus2-s2.0-85082061861
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.3390/biology9030052
dc.identifier.urihttps://hdl.handle.net/20.500.14854/5645
dc.identifier.volume9
dc.identifier.wosWOS:000525146100008
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherMdpi
dc.relation.ispartofBiology-Basel
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20251020
dc.subjectmicroRNA
dc.subjectin situ hybridization
dc.subjectprostate cancer
dc.subjectWnt-11
dc.subjectmiR-21
dc.titleUpregulated Wnt-11 and miR-21 Expression Trigger Epithelial Mesenchymal Transition in Aggressive Prostate Cancer Cells
dc.typeArticle

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