Abstract
In the present study, we found that CBD inhibited U87-MG and T98G cell proliferation and invasiveness in vitro and caused a decrease in the expression of a set of proteins specifically involved in growth, invasion and angiogenesis. In addition, CBD treatment caused a dose-related down-regulation of ERK and Akt prosurvival signaling pathways in U87-MG and T98G cells and decreased hypoxia inducible factor HIF-1α expression in U87-MG cells. Taken together, these results provide new insights into the antitumor action of CBD, showing that this cannabinoid affects multiple tumoral features and molecular pathways. As CBD is a non-psychoactive phytocannabinoid that appears to be devoid of side effects, our results support its exploitation as an effective anti-cancer drug in the management of gliomas.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents / pharmacology*
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Blotting, Western
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Cannabidiol / pharmacology*
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Cell Line, Tumor
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Cell Movement / drug effects*
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Cell Proliferation / drug effects*
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Cell Survival / drug effects
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Dose-Response Relationship, Drug
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Extracellular Signal-Regulated MAP Kinases / metabolism
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Glioma / drug therapy
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Glioma / metabolism
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Glioma / pathology
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Humans
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Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
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Neoplasm Invasiveness
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Proteome / metabolism
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Proteomics / methods
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Proto-Oncogene Proteins c-akt / metabolism
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Signal Transduction / drug effects
Substances
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Antineoplastic Agents
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HIF1A protein, human
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Hypoxia-Inducible Factor 1, alpha Subunit
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Proteome
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Cannabidiol
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Proto-Oncogene Proteins c-akt
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Extracellular Signal-Regulated MAP Kinases
Grants and funding
This work was supported by a grant from University of Milan-F.I.R.S.T 2008. GW Pharmaceuticals funded part of the research. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.