Thio-Cl-IB-MECA, a novel A3 adenosine receptor agonist, suppresses angiogenesis by regulating PI3K/AKT/mTOR and ERK signaling in endothelial cells.
Biochem Biophys Res Commun
; 437(1): 79-86, 2013 Jul 19.
Article
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| MEDLINE
| ID: mdl-23791876
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.
Palabras clave
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
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Adenosina
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Neovascularización Fisiológica
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Fosfatidilinositol 3-Quinasas
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Quinasas MAP Reguladas por Señal Extracelular
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Proteínas Proto-Oncogénicas c-akt
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Serina-Treonina Quinasas TOR
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Células Endoteliales de la Vena Umbilical Humana
Límite:
Animals
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Humans
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
2013
Tipo del documento:
Article