Quinoides and VEGFR2 TKIs influence the fate of hepatocellular carcinoma and its cancer stem cells

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dc.citation.epage87en_US
dc.citation.issueNumber1en_US
dc.citation.spage81en_US
dc.citation.volumeNumber8en_US
dc.contributor.authorKahraman, D. C.en_US
dc.contributor.authorHanquet, G.en_US
dc.contributor.authorJeanmart, L.en_US
dc.contributor.authorLanners, S.en_US
dc.contributor.authorŠramel, P.en_US
dc.contributor.authorBoháč, A.en_US
dc.contributor.authorCetin-Atalay, R.en_US
dc.date.accessioned2018-04-12T11:07:18Z
dc.date.available2018-04-12T11:07:18Z
dc.date.issued2017en_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractBioactivities of quinoides 1–5 and VEGFR2 TKIs 6–10 in hepatocellular cancer (HCC) and cancer stem cells (HCSCs) were studied. The compounds exhibited IC50 values in μM concentrations in HCC cells. Quinoide 3 was able to eradicate cancer stem cells, similar to the action of the stem cell inhibitor DAPT. However, the more cytotoxic VEFGR TKIs (IC50: 0.4–3.0 μM) including sorafenib, which is the only FDA approved drug for the treatment of HCC, enriched the hepatocellular cancer stem cell population by 2–3 fold after treatment. An aggressiveness factor (AF) was proposed to quantify the characteristics of drug candidates for their ability to eradicate the CSC subpopulation. Considering the tumour heterogeneity and marker positive cancer stem cell like subpopulation enrichment upon treatments in patients, this study emphasises the importance of the chemotherapeutic agent choice acting differentially on all the subpopulations including marker-positive CSCs.en_US
dc.description.provenanceMade available in DSpace on 2018-04-12T11:07:18Z (GMT). No. of bitstreams: 1 bilkent-research-paper.pdf: 179475 bytes, checksum: ea0bedeb05ac9ccfb983c327e155f0c2 (MD5) Previous issue date: 2017en
dc.identifier.doi10.1039/c6md00392cen_US
dc.identifier.issn2040-2503
dc.identifier.urihttp://hdl.handle.net/11693/37249
dc.language.isoEnglishen_US
dc.publisherRoyal Society of Chemistryen_US
dc.relation.isversionofhttp://dx.doi.org/10.1039/c6md00392cen_US
dc.source.titleMedChemCommen_US
dc.subjectBeta cateninen_US
dc.subjectCD133 antigenen_US
dc.subjectEpithelial cell adhesion moleculeen_US
dc.subjectProtein p53en_US
dc.subjectProtein tyrosine kinase inhibitoren_US
dc.subjectQuinoideen_US
dc.subjectSorafeniben_US
dc.subjectThy 1 antigenen_US
dc.subjectTranscription factoren_US
dc.subjectTranscription factoren_US
dc.subjectUnclassified drugen_US
dc.subjectVasculotropin receptor 2en_US
dc.subjectVimentinen_US
dc.subjectAntineoplastic activityen_US
dc.subjectCancer cellen_US
dc.subjectCancer stem cellen_US
dc.subjectCell populationen_US
dc.subjectCell subpopulationen_US
dc.subjectConcentration responseen_US
dc.subjectDrug approvalen_US
dc.subjectDrug cytotoxicityen_US
dc.subjectDrug efficacyen_US
dc.subjectDrug mechanismen_US
dc.subjectDrug structureen_US
dc.subjectDrug synthesisen_US
dc.subjectEpithelial mesenchymal transitionen_US
dc.subjectGeneen_US
dc.subjectHumanen_US
dc.subjectHuman cellen_US
dc.subjectIC50en_US
dc.subjectLiver cell carcinomaen_US
dc.subjectProtein expressionen_US
dc.subjectTP53 geneen_US
dc.titleQuinoides and VEGFR2 TKIs influence the fate of hepatocellular carcinoma and its cancer stem cellsen_US
dc.typeArticleen_US

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