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-1a 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.
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