Quinoides and VEGFR2 TKIs influence the fate of hepatocellular carcinoma and its cancer stem cells
dc.citation.epage | 87 | en_US |
dc.citation.issueNumber | 1 | en_US |
dc.citation.spage | 81 | en_US |
dc.citation.volumeNumber | 8 | en_US |
dc.contributor.author | Kahraman, D. C. | en_US |
dc.contributor.author | Hanquet, G. | en_US |
dc.contributor.author | Jeanmart, L. | en_US |
dc.contributor.author | Lanners, S. | en_US |
dc.contributor.author | Šramel, P. | en_US |
dc.contributor.author | Boháč, A. | en_US |
dc.contributor.author | Cetin-Atalay, R. | en_US |
dc.date.accessioned | 2018-04-12T11:07:18Z | |
dc.date.available | 2018-04-12T11:07:18Z | |
dc.date.issued | 2017 | en_US |
dc.department | Department of Molecular Biology and Genetics | en_US |
dc.description.abstract | Bioactivities 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.provenance | Made 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: 2017 | en |
dc.identifier.doi | 10.1039/c6md00392c | en_US |
dc.identifier.issn | 2040-2503 | |
dc.identifier.uri | http://hdl.handle.net/11693/37249 | |
dc.language.iso | English | en_US |
dc.publisher | Royal Society of Chemistry | en_US |
dc.relation.isversionof | http://dx.doi.org/10.1039/c6md00392c | en_US |
dc.source.title | MedChemComm | en_US |
dc.subject | Beta catenin | en_US |
dc.subject | CD133 antigen | en_US |
dc.subject | Epithelial cell adhesion molecule | en_US |
dc.subject | Protein p53 | en_US |
dc.subject | Protein tyrosine kinase inhibitor | en_US |
dc.subject | Quinoide | en_US |
dc.subject | Sorafenib | en_US |
dc.subject | Thy 1 antigen | en_US |
dc.subject | Transcription factor | en_US |
dc.subject | Transcription factor | en_US |
dc.subject | Unclassified drug | en_US |
dc.subject | Vasculotropin receptor 2 | en_US |
dc.subject | Vimentin | en_US |
dc.subject | Antineoplastic activity | en_US |
dc.subject | Cancer cell | en_US |
dc.subject | Cancer stem cell | en_US |
dc.subject | Cell population | en_US |
dc.subject | Cell subpopulation | en_US |
dc.subject | Concentration response | en_US |
dc.subject | Drug approval | en_US |
dc.subject | Drug cytotoxicity | en_US |
dc.subject | Drug efficacy | en_US |
dc.subject | Drug mechanism | en_US |
dc.subject | Drug structure | en_US |
dc.subject | Drug synthesis | en_US |
dc.subject | Epithelial mesenchymal transition | en_US |
dc.subject | Gene | en_US |
dc.subject | Human | en_US |
dc.subject | Human cell | en_US |
dc.subject | IC50 | en_US |
dc.subject | Liver cell carcinoma | en_US |
dc.subject | Protein expression | en_US |
dc.subject | TP53 gene | en_US |
dc.title | Quinoides and VEGFR2 TKIs influence the fate of hepatocellular carcinoma and its cancer stem cells | en_US |
dc.type | Article | en_US |
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