About: Mechanisms of ellipticine-mediated resistance in UKF-NB-4 neuroblastoma cells     Goto   Sponge   NotDistinct   Permalink

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  • Anotace v jazyce originálu:Most high-risk neuroblastomas develop resistance to cytostatics and therefore there is a need to develop new drugs. In previous studies, we found that ellipticine induces apoptosis in human neuroblastoma cells. We also investigated whether ellipticine was able to induce resistance in the UKF-NB-4 neuroblastoma line and concluded that it may be possible after long-term treatment with increasing concentrations of ellipticine. The aim of the present study was to investigate the mechanisms responsible for ellipticine resistance. To elucidate the mechanisms involved, we used the ellipticine-resistant subline UKF-NB-4ELLI and performed comparative genomic hybridization, multicolor and interphase FISH, expression microarray, real-time RT-PCR, flow cytometry and western blotting analysis of proteins. On the basis of our results, it appears that ellipticine resistance in neuroblastoma is caused by a combination of overexpression of Bcl-2, efflux or degradation of the drug and downregulation of topoisomerases. Other mechanisms, such as upregulation of enzymes involved in oxidative phosphorylation, cellular respiration, V-ATPases, aerobic respiration or spermine synthetase, as well as reduced growth rate, may also be involved. Some changes are expressed at the DNA level, including gains, amplifications or deletions. The present study demonstrates that resistance to ellipticine is caused by a combination of mechanisms.
  • Anotace v jazyce originálu:Most high-risk neuroblastomas develop resistance to cytostatics and therefore there is a need to develop new drugs. In previous studies, we found that ellipticine induces apoptosis in human neuroblastoma cells. We also investigated whether ellipticine was able to induce resistance in the UKF-NB-4 neuroblastoma line and concluded that it may be possible after long-term treatment with increasing concentrations of ellipticine. The aim of the present study was to investigate the mechanisms responsible for ellipticine resistance. To elucidate the mechanisms involved, we used the ellipticine-resistant subline UKF-NB-4ELLI and performed comparative genomic hybridization, multicolor and interphase FISH, expression microarray, real-time RT-PCR, flow cytometry and western blotting analysis of proteins. On the basis of our results, it appears that ellipticine resistance in neuroblastoma is caused by a combination of overexpression of Bcl-2, efflux or degradation of the drug and downregulation of topoisomerases. Other mechanisms, such as upregulation of enzymes involved in oxidative phosphorylation, cellular respiration, V-ATPases, aerobic respiration or spermine synthetase, as well as reduced growth rate, may also be involved. Some changes are expressed at the DNA level, including gains, amplifications or deletions. The present study demonstrates that resistance to ellipticine is caused by a combination of mechanisms. (en)
Title
  • Mechanisms of ellipticine-mediated resistance in UKF-NB-4 neuroblastoma cells
  • Mechanisms of ellipticine-mediated resistance in UKF-NB-4 neuroblastoma cells (en)
skos:prefLabel
  • Mechanisms of ellipticine-mediated resistance in UKF-NB-4 neuroblastoma cells
  • Mechanisms of ellipticine-mediated resistance in UKF-NB-4 neuroblastoma cells (en)
skos:notation
  • RIV/00216208:11310/12:10123193!RIV13-GA0-11310___
http://linked.open...avai/predkladatel
http://linked.open...avai/riv/aktivita
http://linked.open...avai/riv/aktivity
  • I, P(GAP301/10/0356), Z(MSM0021620813)
http://linked.open...iv/cisloPeriodika
  • 2
http://linked.open...vai/riv/dodaniDat
http://linked.open...aciTvurceVysledku
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  • 149175
http://linked.open...ai/riv/idVysledku
  • RIV/00216208:11310/12:10123193
http://linked.open...riv/jazykVysledku
http://linked.open.../riv/klicovaSlova
  • cisplatin; doxorubicin; chemotherapy; lines; expression; DNA; antitumor agents; multidrug-resistant; anticancer drug ellipticine; comparative genomic hybridization (en)
http://linked.open.../riv/klicoveSlovo
http://linked.open...odStatuVydavatele
  • US - Spojené státy americké
http://linked.open...ontrolniKodProRIV
  • [C038E3F24E17]
http://linked.open...i/riv/nazevZdroje
  • Cancer Science
http://linked.open...in/vavai/riv/obor
http://linked.open...ichTvurcuVysledku
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http://linked.open...vavai/riv/projekt
http://linked.open...UplatneniVysledku
http://linked.open...v/svazekPeriodika
  • 103
http://linked.open...iv/tvurceVysledku
  • Eckschlager, Tomáš
  • Hraběta, Jan
  • Procházka, Pavel
  • Poljaková, Jitka
  • Stiborová, Marie
  • Zemanová, Zuzana
  • Bunček, Martin
  • Libra, Antonín
  • Hřebačková, Jana
http://linked.open...ain/vavai/riv/wos
  • 000299734000026
http://linked.open...n/vavai/riv/zamer
issn
  • 1347-9032
number of pages
http://bibframe.org/vocab/doi
  • 10.1111/j.1349-7006.2011.02137.x
http://localhost/t...ganizacniJednotka
  • 11310
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