Abstract
Angiogenesis is the formation of blood vessels from pre-existing vasculature. Excessive or uncontrolled angiogenesis is a major contributor to many pathological conditions whereas inhibition of aberrant angiogenesis is beneficial to patients with pathological angiogenesis. Catunaregin is a core of novel marine compound isolated from mangrove associate. The potential anti-angiogenesis of catunaregin was investigated in human umbilical vein endothelial cells (HUVECs) and zebrafish. HUVECs were treated with different concentrations of catunaregin in the presence or absence of VEGF. The angiogenic phenotypes including cell invasion cell migration and tube formation were evaluated following catunaregin treatment in HUVECs. The possible involvement of AKT, eNOS and ERK1/2 in catunaregin-induced anti-angiogenesis was explored using Western blotting. The anti-angiogenesis of catunaregin was further tested in the zebrafish embryo neovascularization and caudal fin regeneration assays. We found that catunaregin dose-dependently inhibited angiogenesis in both HUVECs and zebrafish embryo neovascularization and zebrafish caudal fin regeneration assays. In addition, catunaregin significantly decreased the phosphorylation of Akt and eNOS, but not the phosphorylation of ERK1/2. The present work demonstrates that catunaregin exerts the anti-angiogenic activity at least in part through the regulation of the Akt and eNOS signaling pathways.
Highlights
Angiogenesis is the formation of blood vessels from pre-existing vasculature
Our experimental results demonstrated that the catunaregin could significantly inhibit vascular endothelial growth factor (VEGF)-induced different angiogenic phenotypes of human umbilical vein endothelial cells (HUVECs) in vitro and the vessel formation in transgenic zebrafish
To further investigate the underlying mechanisms behind the anti-angiogenic property of catunaregin, we examined angiogenesis-related signaling pathways in HUVECs
Summary
Angiogenesis is the formation of blood vessels from pre-existing vasculature. The process of angiogenesis is very complex and tightly controlled under physiological conditions. Great efforts have been placed on developing drugs that attack and kill cancer cells. Cytotoxic agents have significantly improved cancer survival, these conventional anti-cancer drugs often cause serious side effects, chemo- and radio-resistance, disease relapse and metastases. Through stimulating blood vessel growth from nearby pre-existing capillaries, tumors achieve sufficient blood supply for cancer cell progression and metastasis [2]. Intensive efforts are needed to develop novel anti-angiogenic agents, especially small molecule targeting the tumor vasculature [3]. VEGF signaling pathway is an attractive target for the development of anti-angiogenesis inhibitors. Since angiogenesis plays an important pathological role in the progress of a wide range of diseases, our findings provide a rationale for future development of this compound as a potential drug or chemopreventive supplement to target diseases with excessive angiogenesis
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