Kahraman, D. C.Hanquet, G.Jeanmart, L.Lanners, S.Šramel, P.Boháč, A.Cetin-Atalay, R.2018-04-122018-04-1220172040-2503http://hdl.handle.net/11693/37249Bioactivities 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.EnglishBeta cateninCD133 antigenEpithelial cell adhesion moleculeProtein p53Protein tyrosine kinase inhibitorQuinoideSorafenibThy 1 antigenTranscription factorTranscription factorUnclassified drugVasculotropin receptor 2VimentinAntineoplastic activityCancer cellCancer stem cellCell populationCell subpopulationConcentration responseDrug approvalDrug cytotoxicityDrug efficacyDrug mechanismDrug structureDrug synthesisEpithelial mesenchymal transitionGeneHumanHuman cellIC50Liver cell carcinomaProtein expressionTP53 geneArticle10.1039/c6md00392c