Inhibition of Midkine Suppresses Prostate Cancer CD133+ Stem Cell Growth and Migration

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dc.authoridSERTTAS, RIZA/0000-0002-7493-0388
dc.authoridDoganlar, Zeynep Banu/0000-0002-1365-9897
dc.authoridDoganlar, Oguzhan/0000-0003-2654-7269
dc.authoridERDOGAN, SUAT/0000-0002-6823-6293
dc.authorwosidSERTTAS, RIZA/AAG-7463-2020
dc.authorwosidDoganlar, Zeynep Banu/B-4845-2008
dc.authorwosidDoğanlar, Oğuzhan/A-2315-2019
dc.contributor.authorErdogan, Suat
dc.contributor.authorDoganlar, Zeynep B.
dc.contributor.authorDoganlar, Oguzhan
dc.contributor.authorTurkekul, Kader
dc.contributor.authorSerttas, Riza
dc.date.accessioned2024-06-12T10:55:58Z
dc.date.available2024-06-12T10:55:58Z
dc.date.issued2017
dc.departmentTrakya Üniversitesien_US
dc.description.abstractBackground: Midkine (MDK) is a tumor-promoting factor that is often overexpressed in various human carcinomas, and the role of MDK has not yet been fully investigated in prostate cancer stem cells. Materials and Methods: Prostate cancer CD133(+) stem cells (PCSCs) were isolated from human castration-resistant PC3 cells. PCSCs were treated with different concentrations of MDK inhibitor, iMDK, for 24-72 hours. The IC50 values were determined by the MTT test. Endogenous MDK messenger RNA expression was knocked down by small interfering RNA. Quantitative reverse transcription polymerase chain reaction, Western blot analyses and image-based cytometry were used to investigate apoptosis and cell cycle progression as well as their underlying molecular mechanisms. Cell migration was evaluated by the wound healing test. Results: iMDK caused dose- and time-dependent inhibition of PCSC survival. Similar growth inhibition was also obtained by small interfering RNA mediated knockdown of endogenous MDK expression. iMDK was shown to preferentially induce cell cycle arrest at the S and G2/M phases. Suppressed PCSC growth was also accompanied by increases in p53 and the cell cycle inhibitor p21 genes. Combinatorial treatment of iMDK with docetaxel significantly inhibited cell proliferation versus either of the agents used alone. Inhibition of MDK expression strongly suppressed the migration of PCSCs compared to untreated and docetaxel-treated cells. iMDK and the knockdown of MDK decreased p-Akt and significantly upregulated the expression of PI3K/phosphatase/tensin homolog. Conclusions: Our data indicate that MDK plays a crucial role in controlling PCSC proliferation and migration. Therefore, suppression of endogenous expression of MDK would, in combination with traditional chemotherapy drugs, be a potential treatment for PCSCs.en_US
dc.description.sponsorshipTrakya University Research Project Foundation, Edirne, Turkey [2015-65]en_US
dc.description.sponsorshipThis study was funded by the Trakya University Research Project Foundation (Project number: 2015-65), Edirne, Turkey.en_US
dc.identifier.endpage309en_US
dc.identifier.issn0002-9629
dc.identifier.issn1538-2990
dc.identifier.issue3en_US
dc.identifier.pmid28918838en_US
dc.identifier.scopus2-s2.0-85030417767en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage299en_US
dc.identifier.urihttps://hdl.handle.net/20.500.14551/19620
dc.identifier.volume354en_US
dc.identifier.wosWOS:000410832600015en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofAmerican Journal Of The Medical Sciencesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCD133(+)en_US
dc.subjectImdken_US
dc.subjectMidkineen_US
dc.subjectProstate Canceren_US
dc.subjectStem Cellsen_US
dc.subjectEpithelial-Mesenchymal Transitionen_US
dc.subjectTumor-Growthen_US
dc.subjectFunctional Receptorsen_US
dc.subjectDrug-Resistanceen_US
dc.subjectLung-Canceren_US
dc.subjectPtenen_US
dc.subjectExpressionen_US
dc.subjectMetastasisen_US
dc.subjectSurvivalen_US
dc.subjectPathwayen_US
dc.titleInhibition of Midkine Suppresses Prostate Cancer CD133+ Stem Cell Growth and Migrationen_US
dc.typeArticleen_US

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