Effect of SIRT1 activators and inhibitors on CD44(+)/CD133(+)-enriched non-small cell lung cancer cells

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dc.contributor.authorEroglu, Zuhal
dc.contributor.authorErdem, Ceren
dc.contributor.authorOktem, Gulperi
dc.contributor.authorCetintas, Vildan Bozok
dc.contributor.authorDuzgun, Zekeriya
dc.date.accessioned2020-12-01T11:59:14Z
dc.date.available2020-12-01T11:59:14Z
dc.date.issued2020
dc.departmentEge Üniversitesien_US
dc.description.abstractLung cancer is one of the most commonly diagnosed cancers and it is associated with high rates of morbidity and mortality. Metastasis and relapse of the tumor depend on the survival and proliferation of lung cancer stem cells (LCSCs). the ability to identify CSCs may prevent recurrence and lead to more effective treatments. Sirtuins are a group of deacetylases that include seven variants (SIRT1-7), with sirtuin 1 (SIRT1) being the most intensively investigated. Evidence suggests thatSIRT1is both a tumor-suppressor gene and an oncogene. SIRT1 can deacetylate the tumor-suppressor protein p53 to decrease its activity. SIRT1 activators increase the deacetylation of p53, whereas SIRT1 inhibitors can stimulate p53 by inhibiting deacetylation. in the present study, CD44(+)and CD133(+)-enriched A549 (non-small cell lung cancer) cells collected using the CD44 and CD133 CSC surface markers by fluorescence-activated cell sorting method were treated with SIRT1 inhibitors (tenovin-6 and sirtinol) and SIRT1 activators (resveratrol and SRT1720), and their effects on apoptosis, as well as the mRNA and protein expression of SIRT1 and p53 were investigated. of these agents, it was found that resveratrol increased p53 expression by 4.1-fold, decreased SIRT1 expression by 0.2-fold, and it was the most potent inducer of apoptosis.en_US
dc.description.sponsorshipScientific Research Projects Coordination Unit of Ege University [15-TIP-061]en_US
dc.description.sponsorshipThe current study was supported by the Scientific Research Projects Coordination Unit of Ege University (grant no. 15-TIP-061).en_US
dc.identifier.doi10.3892/mmr.2020.11113en_US
dc.identifier.endpage581en_US
dc.identifier.issn1791-2997
dc.identifier.issn1791-3004
dc.identifier.issue1en_US
dc.identifier.pmid32377734en_US
dc.identifier.scopus2-s2.0-85084440892en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage575en_US
dc.identifier.urihttps://doi.org/10.3892/mmr.2020.11113
dc.identifier.urihttps://hdl.handle.net/11454/62208
dc.identifier.volume22en_US
dc.identifier.wosWOS:000542289500061en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpandidos Publ Ltden_US
dc.relation.ispartofMolecular Medicine Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectcancer stem cellsen_US
dc.subjectlung canceren_US
dc.subjectsirtuin 1en_US
dc.subjectp53en_US
dc.subjectresveratrolen_US
dc.titleEffect of SIRT1 activators and inhibitors on CD44(+)/CD133(+)-enriched non-small cell lung cancer cellsen_US
dc.typeArticleen_US

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