| Cannabidiol inhibits angiogenesis by multiple mechanisms. | |
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MedLine Citation:
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PMID: 22624859 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND AND PURPOSE: Several studies have demonstrated anti-proliferative and pro-apoptotic actions of cannabinoids on various tumours, together with their anti-angiogenic properties. The non-psychoactive cannabinoid cannabidiol (CBD) effectively inhibits the growth of different types of tumours in vitro and in vivo and down-regulates some pro-angiogenic signals produced by glioma cells. As its anti-angiogenic properties have not been thoroughly investigated to date, and given its very favourable pharmacological and toxicological profile, here, we evaluated the ability of CBD to modulate tumour angiogenesis. EXPERIMENTAL APPROACH: Firstly, we evaluated the effect of CBD on human umbilical vein endothelial cell (HUVEC) proliferation and viability - through [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay and FACS analysis - and in vitro motility - both in a classical Boyden chamber test and in a wound-healing assay. We next investigated CBD effects on different angiogenesis-related proteins released by HUVECs, using an angiogenesis array kit and an ELISA directed at MMP2. Then we evaluated its effects on in vitro angiogenesis in treated HUVECs invading a Matrigel layer and in HUVEC spheroids embedded into collagen gels, and further characterized its effects in vivo using a Matrigel sponge model of angiogenesis in C57/BL6 mice. KEY RESULTS: CBD induced HUVEC cytostasis without inducing apoptosis, inhibited HUVEC migration, invasion and sprouting in vitro, and angiogenesis in vivo in Matrigel sponges. These effects were associated with the down-modulation of several angiogenesis-related molecules. CONCLUSIONS AND IMPLICATIONS: This study reveals that CBD inhibits angiogenesis by multiple mechanisms. Its dual effect on both tumour and endothelial cells supports the hypothesis that CBD has potential as an effective agent in cancer therapy. |
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Authors:
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M Solinas; P Massi; A R Cantelmo; M G Cattaneo; R Cammarota; D Bartolini; V Cinquina; M Valenti; L M Vicentini; D M Noonan; A Albini; D Parolaro |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: British journal of pharmacology Volume: 167 ISSN: 1476-5381 ISO Abbreviation: Br. J. Pharmacol. Publication Date: 2012 Nov |
Date Detail:
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Created Date: 2012-10-22 Completed Date: 2013-03-25 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 7502536 Medline TA: Br J Pharmacol Country: England |
Other Details:
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Languages: eng Pagination: 1218-31 Citation Subset: IM |
Copyright Information:
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© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society. |
Affiliation:
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Department of Biomedical, Computer and Communication Sciences, University of Insubria, Busto Arsizio (VA), Italy. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angiogenesis Inhibitors
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pharmacology,
therapeutic use* Animals Cannabidiol / pharmacology, therapeutic use* Cell Movement / drug effects Heparin Human Umbilical Vein Endothelial Cells Humans Male Mice Mice, Inbred C57BL Neovascularization, Pathologic / chemically induced, drug therapy* Tumor Necrosis Factor-alpha Vascular Endothelial Growth Factor A |
| Chemical | |
Reg. No./Substance:
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0/Angiogenesis Inhibitors; 0/Tumor Necrosis Factor-alpha; 0/Vascular Endothelial Growth Factor A; 13956-29-1/Cannabidiol; 9005-49-6/Heparin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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