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dc.contributor.authorArisan, Elif Damla
dc.contributor.authorRencuzogullari, Ozge
dc.contributor.authorKeskin, Buse
dc.contributor.authorGrant, Guy H.
dc.contributor.authorUysal-Onganer, Pinar
dc.date.accessioned2020-09-14T09:29:15Z
dc.date.available2020-06-27T00:00:00Z
dc.date.available2020-09-14T09:29:15Z
dc.date.issued2020-06-27
dc.identifier.citationArisan ED, Rencuzogullari O, Keskin B, Grant GH, Uysal-Onganer P (2020) 'Inhibition on JNK mimics silencing of Wnt-11 mediated cellular response in androgen-independent prostate cancer cells', Biology, 9 (7), pp.142-.en_US
dc.identifier.issn2079-7737
dc.identifier.pmid32605008
dc.identifier.doi10.3390/biology9070142
dc.identifier.urihttp://hdl.handle.net/10547/624510
dc.description.abstractProstate cancer (PCa) is one of the most common cancers among men, and one of the leading causes of cancer death for men. The c-Jun N-terminal kinase (JNK) pathway is required for several cellular functions, such as survival, proliferation, differentiation, and migration. Wnt-11, a member of the Wnt family, has been identified for its upregulation in PCa; however, downstream signalling of Wnt-11 remains to be fully characterized. In this study, we investigated the role of the JNK pathway as a potential downstream factor for Wnt-11 signalling. For this purpose, LNCaP, DU145, and PC-3 PCa cells and normal epithelial PNT1A cells were treated with a specific JNK kinase inhibitor: JNKVIII. Our results showed that JNK inhibition decreased mitochondrial membrane potential and promoted cell death in a cell type-dependent manner. We found that JNK inhibition led to an increase in autophagy and prevented epithelial-mesenchymal transition (EMT) in independently growing androgen cells. JNK inhibition and the silencing of Wnt-11 showed similar responses in DU145 and PC-3 cells and decreased metastasis-related biomarkers, cell migration, and invasion. Overall, our results suggest that JNK signalling plays a significant role in the pathophysiology of PCa by mediating Wnt-11 induced signals. Our data highlights that both the JNK pathway and Wnt-11 could be a useful therapeutic target for the combinatory application of current PCa.en_US
dc.language.isoenen_US
dc.publisherMDPIen_US
dc.relation.urlhttps://www.mdpi.com/2079-7737/9/7/142en_US
dc.rightsGreen - can archive pre-print and post-print or publisher's version/PDF
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectc-Jun signallingen_US
dc.subjectprostate canceren_US
dc.subjectapoptosisen_US
dc.subjectWnt-11en_US
dc.subjectneuroendocrine-like differentiationen_US
dc.titleInhibition on JNK mimics silencing of Wnt-11 mediated cellular response in androgen-independent prostate cancer cellsen_US
dc.typeArticleen_US
dc.identifier.eissn2079-7737
dc.contributor.departmentGebze Technical Universityen_US
dc.contributor.departmentIstanbul Kultur Universityen_US
dc.contributor.departmentUniversity of Bedfordshireen_US
dc.contributor.departmentUniversity of Westminsteren_US
dc.identifier.journalBiologyen_US
dc.date.updated2020-09-14T09:24:36Z
dc.description.noteopen access


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