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.
Highlights
Malignant gliomas are among the most rapidly growing and devastating neoplasms with poor prognosis
Among the cellular signals that prompt tumor cells to egress from the tumor mass and are associated with enhanced glioma invasiveness, an important role is played by the high expression levels of matrix metalloproteinases (MMPs), a family of enzymes promoting tissue breakdown and remodelling through the degradation of extracellular matrix (ECM) [2], as well as the expression of several other proteases and factors [3]
Effect of CBD on Glioma Cell Invasion The matrigel invasion assay was carried out to examine the effect of CBD on the invasiveness of U87-MG and T98G glioma cells
Summary
Malignant gliomas are among the most rapidly growing and devastating neoplasms with poor prognosis. Gliomas rarely metastasize out of the central nervous system, but their aggressive invasion of normal peritumoral tissue makes surgical removal virtually impossible [1]. Among the cellular signals that prompt tumor cells to egress from the tumor mass and are associated with enhanced glioma invasiveness, an important role is played by the high expression levels of matrix metalloproteinases (MMPs), a family of enzymes promoting tissue breakdown and remodelling through the degradation of extracellular matrix (ECM) [2], as well as the expression of several other proteases and factors [3]. It can be suggested that controlling the expression of all of these factors may represent a promising therapeutic strategy for treating gliomas
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