Zvýšená exprese P-glykoproteinu uděluje leukemickým buňkám rezistenci vůči agonistovi A3 adenosinového receptoru (A3AR) 2-chlor-N6-(3-jodobenzyl)-adenosin-5'-N-methyluronamid (Cl-IB-MECA)

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F08%3A00006192" target="_blank" >RIV/61989592:15110/08:00006192 - 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

P-glycoprotein overexpression confers resistance to A3 adenosine receptor agonists 2-chloro-N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA) in human leukemia cells

Popis výsledku v původním jazyce

BACKGROUND: 2-chloro-N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA) the A3 adenosine receptor (A3AR) agonist has been implicated in modulation of cell proliferation and cell death. Effects of Cl-IB-MECA strongly depend on the concentrationused. Thus, nanomolar concentrations of Cl-IB-MECA stimulate cell proliferation and protect cells from death in some experimental models. On the other hand, micromolar concentrations of Cl-IB-MECA are cytotoxic and induce apoptosis itself. Interestingly, antagonistic effects of Cl-IB-MECA were attributed to the same signalling pathway, which is triggered upon ligation of A3AR. We studied cytotoxic effects of Cl-IB-MECA in K562/Dox cell line, which exhibits multidrug resistance phenotype. METHODS: K562/Dox cells were derived from K562 cell line, by long-term cultivation in the presence of increasing concentration of doxorubicin. K562/Dox is resistant to doxorubicin and also to other drugs due to P-glycoprotein (ABCB1, MDR1) overexperssi

Název v anglickém jazyce

P-glycoprotein overexpression confers resistance to A3 adenosine receptor agonists 2-chloro-N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA) in human leukemia cells

Popis výsledku anglicky

BACKGROUND: 2-chloro-N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA) the A3 adenosine receptor (A3AR) agonist has been implicated in modulation of cell proliferation and cell death. Effects of Cl-IB-MECA strongly depend on the concentrationused. Thus, nanomolar concentrations of Cl-IB-MECA stimulate cell proliferation and protect cells from death in some experimental models. On the other hand, micromolar concentrations of Cl-IB-MECA are cytotoxic and induce apoptosis itself. Interestingly, antagonistic effects of Cl-IB-MECA were attributed to the same signalling pathway, which is triggered upon ligation of A3AR. We studied cytotoxic effects of Cl-IB-MECA in K562/Dox cell line, which exhibits multidrug resistance phenotype. METHODS: K562/Dox cells were derived from K562 cell line, by long-term cultivation in the presence of increasing concentration of doxorubicin. K562/Dox is resistant to doxorubicin and also to other drugs due to P-glycoprotein (ABCB1, MDR1) overexperssi

Druh

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

CEP obor

FD - Onkologie a hematologie

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)

Rok uplatnění

2008

Kód důvěrnosti údajů

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

Název periodika

Purinergic Signalling

ISSN

1573-9538

e-ISSN

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Svazek periodika

4

Číslo periodika v rámci svazku

S1

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

2

Strana od-do

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Kód UT WoS článku

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EID výsledku v databázi Scopus

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