Midkine silencing enhances the anti-prostate cancer stem cell activity of the flavone apigenin: cooperation on signaling pathways regulated by ERK, p38, PTEN, PARP, and NF-?B

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dc.authoridDoganlar, Zeynep Banu/0000-0002-1365-9897
dc.authoridDoganlar, Oguzhan/0000-0003-2654-7269
dc.authoridBilir, Ayhan/0009-0009-9399-5927
dc.authoridERDOGAN, SUAT/0000-0002-6823-6293
dc.authorwosidDoganlar, Zeynep Banu/B-4845-2008
dc.authorwosidDoğanlar, Oğuzhan/A-2315-2019
dc.contributor.authorErdogan, Suat
dc.contributor.authorTurkekul, Kader
dc.contributor.authorDibirdik, Ilker
dc.contributor.authorDoganlar, Zeynep B.
dc.contributor.authorDoganlar, Oguzhan
dc.contributor.authorBilir, Ayhan
dc.date.accessioned2024-06-12T10:52:19Z
dc.date.available2024-06-12T10:52:19Z
dc.date.issued2020
dc.departmentTrakya Üniversitesien_US
dc.description.abstractProstate cancer (PCa) is the most common cancer in men worldwide. Midkine (MK) is overexpressed in PCa, as well as in tumor-initiating cells termed cancer stem cells (CSCs). Apigenin is a dietary flavone with considerable anti-tumor activities. In this study, we explored the possible therapeutic use of MK silencing, apigenin treatment, and a combination of both on human PCa and prostate cancer stem cells (PCSCs). CD44(+)CD133(+) PC3 and CD44(+) LNCaP CSCs were isolated from their parent cell lines. Both MK knockdown and apigenin treatment resulted in loss of cell viability in PCSCs, and these effects were significantly elevated when apigenin was applied with MK silencing. Combined treatment of CD44(+)CD133(+) PC3 cells with apigenin and MK siRNA was also more effective in inducing apoptotic and non-apoptotic cell death when compared with individual applications. Treatment of CD44(+) LNCaP cells with apigenin significantly decreased viability, although the combination treatment did not markedly alter the individual therapy. Molecular events underlying cell cycle arrest and inhibition of the survival, proliferation, and migration of CD44(+)CD133(+) PC3 cells were found to be associated with upregulated p21, p27, Bax, Bid, caspase-3, and caspase-8 expression, as well as downregulated p-p38, p-ERK, NF-kappa B, and PARP. In addition, the combination of apigenin treatment and MK silencing showed better outcomes on the anticancer efficacy of docetaxel in CD44(+)CD133(+) PC3 cells. In conclusion, MK-regulated events are different between PCSCs, and when combined with apigenin plus MK silencing, docetaxel treatment may be a valuable approach for the eradication of PCSCs.en_US
dc.identifier.doi10.1007/s10637-019-00774-8
dc.identifier.endpage263en_US
dc.identifier.issn0167-6997
dc.identifier.issn1573-0646
dc.identifier.issue2en_US
dc.identifier.pmid30993586en_US
dc.identifier.scopus2-s2.0-85064712382en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage246en_US
dc.identifier.urihttps://doi.org/10.1007/s10637-019-00774-8
dc.identifier.urihttps://hdl.handle.net/20.500.14551/18672
dc.identifier.volume38en_US
dc.identifier.wosWOS:000519163000003en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofInvestigational New Drugsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApigeninen_US
dc.subjectMidkineen_US
dc.subjectProstate Canceren_US
dc.subjectCD44en_US
dc.subjectCD133en_US
dc.subjectCancer Stem Cellen_US
dc.subjectDown-Regulationen_US
dc.subjectInhibitionen_US
dc.subjectExpressionen_US
dc.subjectMigrationen_US
dc.subjectApoptosisen_US
dc.subjectActivationen_US
dc.subjectMechanismsen_US
dc.subjectResistanceen_US
dc.subjectIncreasesen_US
dc.subjectPi3k/Akten_US
dc.titleMidkine silencing enhances the anti-prostate cancer stem cell activity of the flavone apigenin: cooperation on signaling pathways regulated by ERK, p38, PTEN, PARP, and NF-?Ben_US
dc.typeArticleen_US

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