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.

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F10%3A10213496" target="_blank" >RIV/61989592:15110/10:10213496 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

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.

Popis výsledku v původním jazyce

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 micromolarconcentration 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.

Název v anglickém jazyce

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.

Popis výsledku anglicky

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 micromolarconcentration 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.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

<a href="/cs/project/NR9482" target="_blank" >NR9482: P-glykoprotein a jeho možný podíl na vzniku resistence vůči imatinibu u buněk exprimujících Bcr-Abl tyrosin kinázu</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2010

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Acta Physiologica

ISSN

1748-1708

e-ISSN

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Svazek periodika

199

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

9

Strana od-do

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Kód UT WoS článku

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EID výsledku v databázi Scopus

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