The natural flavonoid apigenin sensitizes human CD44+ prostate cancer stem cells to cisplatin therapy

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dc.authoridSERTTAS, RIZA/0000-0002-7493-0388
dc.authorwosidSERTTAS, RIZA/AAG-7463-2020
dc.contributor.authorErdogan, Suat
dc.contributor.authorTurkekul, Kader
dc.contributor.authorSerttas, Riza
dc.contributor.authorErdogan, Zeynep
dc.date.accessioned2024-06-12T10:55:59Z
dc.date.available2024-06-12T10:55:59Z
dc.date.issued2017
dc.departmentTrakya Üniversitesien_US
dc.description.abstractProstate cancer (PCa) is the second most common type of cancer and the fifth leading cause of cancerrelated death among men. Development of chemoresistance, tumor relapse and metastasis remain major barriers to effective treatment and all been identified to be associated with cancer stem cells (CSCs). Natural flavonoids such as apigenin have been shown to have the ability to improve the therapeutic efficacy of common chemotherapy agents through CSCs sensitization. Thus, the aim of this study was to evaluate the combination of apigenin with cisplatin on CD44(+) PCa stem cell growth and migration. Platinum-based anti-neoplastic drugs have been used to treat a number of malignancies including PCa. However, acquired resistance and side effects unfortunately have limited cisplatin's use. A CD44(+) subpopulation was isolated from human androgen-independent PC3 PCa cells by using human CD44-PE antibody. IC50 values were determined by MTT test. RT-qPCR, Western blot analyses and image-based cytometer were used to investigate apoptosis, cell cycle and their underlying molecular mechanisms. Cell migration was evaluated by wound healing test. The combination of the IC50 doses of apigenin (15 mu M) and cisplatin (7.5 mu M) for 48 h significantly enhanced cisplatin's cytotoxic and apoptotic effects through downregulation of Bcl-2, sharpin and survivin; and upregulation of caspase-8, Apaf-1 and p53 mRNA expression. The combined therapy suppressed the phosphorylation of p-PI3K and p-Akt, inhibited the protein expression of NF-kB, and downregulated the cell cycle by upregulating p21, as well as cyclin dependent kinases CDK-2, -4, and -6. Apigenin significantly increased the inhibitory effects of cisplatin on cell migration via downregulation of Snail expression. In conclusion, our study showed the possible therapeutic approach of using apigenin to potentially increase the effects of cisplatin by targeting CSCs subset in prostate cancer. (C) 2017 Elsevier Masson SAS. All rights reserved.en_US
dc.identifier.doi10.1016/j.biopha.2017.01.056
dc.identifier.endpage217en_US
dc.identifier.issn0753-3322
dc.identifier.issn1950-6007
dc.identifier.pmid28107698en_US
dc.identifier.scopus2-s2.0-85009454854en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage210en_US
dc.identifier.urihttps://doi.org/10.1016/j.biopha.2017.01.056
dc.identifier.urihttps://hdl.handle.net/20.500.14551/19623
dc.identifier.volume88en_US
dc.identifier.wosWOS:000395528000025en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier France-Editions Scientifiques Medicales Elsevieren_US
dc.relation.ispartofBiomedicine & Pharmacotherapyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCD44(+)en_US
dc.subjectProstate Canceren_US
dc.subjectStem Cellsen_US
dc.subjectApigeninen_US
dc.subjectCisplatinen_US
dc.subjectMolecular-Mechanismsen_US
dc.subjectApoptosisen_US
dc.subjectMigrationen_US
dc.subjectPathwayen_US
dc.subjectCarcinomaen_US
dc.subjectInvasionen_US
dc.subjectReceptoren_US
dc.subjectDrugsen_US
dc.titleThe natural flavonoid apigenin sensitizes human CD44+ prostate cancer stem cells to cisplatin therapyen_US
dc.typeArticleen_US

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