P-glycoprotein mediates resistance to A3 adenosine receptor agonist 2-chloro-N6-(3-iodobenzyl)-adenosine-5?-N-methyluronamide in human leukemia cells

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F12%3A33118945" target="_blank" >RIV/61989592:15110/12:33118945 - isvavai.cz</a>

Result on the web

<a href="http://dx.doi.org/10.1002/jcp.22775" target="_blank" >http://dx.doi.org/10.1002/jcp.22775</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/jcp.22775" target="_blank" >10.1002/jcp.22775</a>

Result language

angličtina

Original language name

P-glycoprotein mediates resistance to A3 adenosine receptor agonist 2-chloro-N6-(3-iodobenzyl)-adenosine-5?-N-methyluronamide in human leukemia cells

Original language description

We studied effects of 2-chloro-N6-(3-iodobenzyl)-adenosine-5?-N-methyluronamide (Cl-IB-MECA) on apoptosis induction in the K562/Dox cell line, which overexpressed P-glycoprotein (P-gp, ABCB1, MDR1). We found that the K562/Dox cell line was significantlymore resistant to Cl-IB-MECA than the maternal cell line K562, which did not express P-gp. Although both cell lines expressed the A3 adenosine receptor (A3AR), cytotoxic effects of Cl-IB-MECA were not prevented by its selective antagonist MRS1523 (3-propyl-6-ethyl-5-[(ethylthio)carbonyl]-2 phenyl-4-propyl-3-pyridine carboxylate). Analysis of cell extracts revealed that the intracellular level of Cl-IB-MECA was significantly lower in the K562/Dox cell line than in the maternal cell line K562. The downregulation of P-gp expression using shRNA targeting ABCB1 gene led to increased intracellular level of Cl-IB-MECA and restored cell sensitivity to this drug. Similarly, valspodar (PSC-833), a specific inhibitor of P-gp, restored sensitivity

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

ED - Physiology

OECD FORD branch

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Project

<a href="/en/project/NR9482" target="_blank" >NR9482: P-glycoprotein and its possible contribution to development of resistance to Imatinib in Bcr-Abl expressing cells</a><br>

Continuities

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

Publication year

2012

Confidentiality

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

Name of the periodical

Journal of Cellular Physiology

ISSN

0021-9541

e-ISSN

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Volume of the periodical

227

Issue of the periodical within the volume

2

Country of publishing house

US - UNITED STATES

Number of pages

10

Pages from-to

676-685

UT code for WoS article

000298092800031

EID of the result in the Scopus database

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