About: Induction of apoptosis by A3 adenosine receptor agonist N6-(3-iodobenzyl)-adenosine-5'-N-methylcarboxamide in human leukemia cells: a possible involvement of intracellular mechanism.     Goto   Sponge   NotDistinct   Permalink

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  • The sensitivity of cancer cells which exhibit multidrug resistance phenotype to A3 adenosine receptor (A3AR) agonist N6-(3-iodobenzyl)-adenosine-5'-N-methylcarboxamide (IB-MECA) was studied. Methods: To establish direct relationship between P-glycoprotein (P-gp, ABCB1, MDR1) and IB-MECA, a straightforward method for precise estimation of intracellular level of this A3AR agonist was developed. Results: We subjected three human leukemia cell lines HL-60, K562, and K562/HHT to the treatment with micromolar concentration of IB-MECA. Despite the fact that all cell lines used expressed A3AR, there was a large difference in sensitivity to IB-MECA. While HL-60 and K562 cells were almost equally sensitive, the K562/HHT cells, which exhibit a multidrug resistance phenotype due to overexpression of P-gp, were significantly more resistant. We found that the intracellular level of IB-MECA in K562/HHT cells was approximately ten times lower than those in HL-60 or K562 cells.
  • The sensitivity of cancer cells which exhibit multidrug resistance phenotype to A3 adenosine receptor (A3AR) agonist N6-(3-iodobenzyl)-adenosine-5'-N-methylcarboxamide (IB-MECA) was studied. Methods: To establish direct relationship between P-glycoprotein (P-gp, ABCB1, MDR1) and IB-MECA, a straightforward method for precise estimation of intracellular level of this A3AR agonist was developed. Results: We subjected three human leukemia cell lines HL-60, K562, and K562/HHT to the treatment with micromolar concentration of IB-MECA. Despite the fact that all cell lines used expressed A3AR, there was a large difference in sensitivity to IB-MECA. While HL-60 and K562 cells were almost equally sensitive, the K562/HHT cells, which exhibit a multidrug resistance phenotype due to overexpression of P-gp, were significantly more resistant. We found that the intracellular level of IB-MECA in K562/HHT cells was approximately ten times lower than those in HL-60 or K562 cells. (en)
Title
  • Induction of apoptosis by A3 adenosine receptor agonist N6-(3-iodobenzyl)-adenosine-5'-N-methylcarboxamide in human leukemia cells: a possible involvement of intracellular mechanism.
  • Induction of apoptosis by A3 adenosine receptor agonist N6-(3-iodobenzyl)-adenosine-5'-N-methylcarboxamide in human leukemia cells: a possible involvement of intracellular mechanism. (en)
skos:prefLabel
  • Induction of apoptosis by A3 adenosine receptor agonist N6-(3-iodobenzyl)-adenosine-5'-N-methylcarboxamide in human leukemia cells: a possible involvement of intracellular mechanism.
  • Induction of apoptosis by A3 adenosine receptor agonist N6-(3-iodobenzyl)-adenosine-5'-N-methylcarboxamide in human leukemia cells: a possible involvement of intracellular mechanism. (en)
skos:notation
  • RIV/61989592:15110/10:10213496!RIV11-MZ0-15110___
http://linked.open...avai/riv/aktivita
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  • P(NR9482), Z(MSM6198959216)
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  • 2
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  • 263471
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  • RIV/61989592:15110/10:10213496
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  • mechanism; intracellular; involvement; possible; cells:; leukemia; human; N6-(3-iodobenzyl)-adenosine-5'-N-methylcarboxamide; agonist; receptor; adenosine; apoptosis; Induction (en)
http://linked.open.../riv/klicoveSlovo
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  • GB - Spojené království Velké Británie a Severního Irska
http://linked.open...ontrolniKodProRIV
  • [E3F8494C2B3E]
http://linked.open...i/riv/nazevZdroje
  • Acta Physiologica
http://linked.open...in/vavai/riv/obor
http://linked.open...ichTvurcuVysledku
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http://linked.open...vavai/riv/projekt
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http://linked.open...v/svazekPeriodika
  • 199
http://linked.open...iv/tvurceVysledku
  • DOLEŽEL, Petr
  • MLEJNEK, Petr
http://linked.open...n/vavai/riv/zamer
issn
  • 1748-1708
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  • 15110
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