eISSN: 1896-9151
ISSN: 1734-1922
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abstract:
Basic research

Differential effect of adenosine on rhabdomyosarcoma migration and proliferation

Maciej Tarnowski
,
Marta Tkacz
,
Katarzyna Piotrowska
,
Katarzyna Zgutka
,
Andrzej Pawlik

Arch Med Sci
Online publish date: 2018/04/26
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Introduction
Adenosine and its receptors are involved deeply in the regulation of tumour biology. Purine nucleotides are released from stressed cells in states of hypoxia or radiochemotherapy-induced cell damage. Adenosine exerts its effect through the P1 family of selective receptors. The purpose of the study was to evaluate the exact role of extracellular role on biology of Rhabdomyosarcoma (RMS) cells.

Material and methods
Series of in vitro studies accompanied by immunohistochemical, RQ-PCR and shRNA methods have characterised adenosine receptor expression on Rhabdomyosarcoma cell lines, normal skeletal muscle and effect of adenosine on Rhabdomyosarcoma growth and migration.

Results
Extracellular adenosine (highest at 50 µM, p < 0.05) and AMP (highest at 300 µM, p < 0.05) markedly enhanced chemotaxis in the Boyden chamber assay The reaction is mostly governed by the A1 receptor, which is greatly overexpressed in Rhabdomyosarcoma as compared with normal skeletal muscle. Cell migration induced by adenosine and AMP is blocked by pertussis toxin, phospholipase C and MAP kinase inhibitor, which demonstrates the importance of these signalling pathways. High doses of adenosine have a detrimental effect on cellular proliferation, in a receptor-independent manner (≥ 500 µM; p < 0.05). The blockage of adenosine transporter by dipyridamole abolishes this effect, indicating involvement of an intrinsic pathway. Further increase of adenosine concentration, induced by deaminase inhibitors, augment the effect.

Conclusions
Our results suggest that adenosine and AMP trigger cell migration by binding to P1 receptors and directing cancer cells to the sites of hypoxia or cellular damage. Specifically by A1 receptor which is overexpressed in RMS.

keywords:

cancer, proliferation, apoptosis, cell migration

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