Abstract
Abstract Angiogenesis is a complex process that involves sprouting of new capillaries from pre-existing blood vessels. Angiogenesis is also involved in many pathological conditions including tumor growth, diabetic retinopathy, psoriasis, rheumatoid arthritis, and atherosclerosis. In cancer, newly formed vessels not only promote tumor growth but also cause the tumor cells to become more malignant and metastatic. Therefore, angiogenesis is an attractive target for the development of a wide variety of therapies, including antitumor agents. A3 adenosine receptor (A3AR) agonists have exhibited anti-proliferative activity against cancer cells. However, anti-angiogenic effects of A3AR agonists in endothelial cells have not been investigated yet. In the present study, the potential anti-angiogenic activity and precise mechanism of action of the A3AR agonist thio-Cl-IB-MECA (TCIM) were investigated in cultured HUVECs and mouse embryonic stem cells/embryonic body (mES/EB) derived endothelial cells. TCIM inhibited migration and tube formation of endothelial cells and markedly decreased ex vivo microvessel sprouting in cultured mouse aortic rings. TCIM also suppressed the expression of the endothelial biomarker platelet endothelial cell adhesion molecule (PECAM) via regulation of PI3K/AKT/mTOR and ERK signaling in mES/EB-derived endothelial cells. Citation Format: Jedo Oh, Gi Dae Kim, Lak Shin Jeong, Sang Kook Lee. Anti-angiogenic activity of Thio-Cl-IB-MECA, a novel A3 adenosine receptor agonist, by regulating of PI3K/AKT/mTOR and ERK signaling pathways in endothelial cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 5567. doi:10.1158/1538-7445.AM2015-5567
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call