Literature DB >> 23791876

Thio-Cl-IB-MECA, a novel A₃ adenosine receptor agonist, suppresses angiogenesis by regulating PI3K/AKT/mTOR and ERK signaling in endothelial cells.

Gi Dae Kim1, Jedo Oh, Lak Shin Jeong, Sang Kook Lee.   

Abstract

Although A₃AR agonists exhibit a variety of biological activities including anticancer effects, their possible anti-angiogenic effects have not yet been investigated. In the present study, we assayed the anti-angiogenic activity of thio-Cl-IB-MECA, a novel A₃AR agonist, in cultured HUVECs and mES/EB-derived endothelial cells. Thio-Cl-IB-MECA inhibited migration and tube formation by endothelial cells and dramatically decreased ex vivo microvessel sprouting in cultured mouse aortic rings. The anti-angiogenic activity of thio-Cl-IB-MECA was associated with suppression of the expression of the endothelial biomarker PECAM via regulation of PI3K/AKT/mTOR and ERK signaling in mES/EB-derived endothelial cells.
Copyright © 2013 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  2-chloro-N(6)-(3-iodobenzyl)-4′-thioadenosine-5′-N-methyluronamide; 2-chloro-N(6)-(3-iodobenzyl)-adenosine-5′-N-methylcarboxamide; A(3) adenosine receptor; A(3)AR; Anti-angiogenesis; Cl-IB-MECA; EB; ERK; Endothelial cells; HUVECs; IB-MECA; N(6)-(3-iodobenzyl)adenosine-5′-N-methyluronamide; PECAM; PI3K; PI3K/AKT/mTOR; Thio-Cl-IB-MECA; embryoid body; extracellular signal-regulated kinase; human umbilical vein endothelial cells; mES; mouse embryonic stem; phosphatidylinositol-3-kinase; platelet/endothelial cell adhesion molecule; thio-Cl-IB-MECA

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Year:  2013        PMID: 23791876     DOI: 10.1016/j.bbrc.2013.06.040

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


  6 in total

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  6 in total

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