Cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in U87-MG and T98G glioma cells through a multitarget effect.

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...

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Main Authors: Marta Solinas, Paola Massi, Valentina Cinquina, Marta Valenti, Daniele Bolognini, Marzia Gariboldi, Elena Monti, Tiziana Rubino, Daniela Parolaro
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24204703/?tool=EBI
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spelling doaj-5f2c082ab39945ca8879f80b014735822021-03-03T22:49:07ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-01810e7691810.1371/journal.pone.0076918Cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in U87-MG and T98G glioma cells through a multitarget effect.Marta SolinasPaola MassiValentina CinquinaMarta ValentiDaniele BologniniMarzia GariboldiElena MontiTiziana RubinoDaniela ParolaroIn 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.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24204703/?tool=EBI
collection DOAJ
language English
format Article
sources DOAJ
author Marta Solinas
Paola Massi
Valentina Cinquina
Marta Valenti
Daniele Bolognini
Marzia Gariboldi
Elena Monti
Tiziana Rubino
Daniela Parolaro
spellingShingle Marta Solinas
Paola Massi
Valentina Cinquina
Marta Valenti
Daniele Bolognini
Marzia Gariboldi
Elena Monti
Tiziana Rubino
Daniela Parolaro
Cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in U87-MG and T98G glioma cells through a multitarget effect.
PLoS ONE
author_facet Marta Solinas
Paola Massi
Valentina Cinquina
Marta Valenti
Daniele Bolognini
Marzia Gariboldi
Elena Monti
Tiziana Rubino
Daniela Parolaro
author_sort Marta Solinas
title Cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in U87-MG and T98G glioma cells through a multitarget effect.
title_short Cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in U87-MG and T98G glioma cells through a multitarget effect.
title_full Cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in U87-MG and T98G glioma cells through a multitarget effect.
title_fullStr Cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in U87-MG and T98G glioma cells through a multitarget effect.
title_full_unstemmed Cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in U87-MG and T98G glioma cells through a multitarget effect.
title_sort cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in u87-mg and t98g glioma cells through a multitarget effect.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2013-01-01
description 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.
url https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24204703/?tool=EBI
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