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β-Caryophyllene Inhibits Cell Proliferation through a Direct Modulation of CB2 Receptors in Glioblastoma Cells

1
Department of Clinical and Experimental Medicine, University of Messina, c/o AOU Policlinico G. Martino, Via C. Valeria Gazzi, 98125 Messina, Italy
2
Department of Human Pathology in Adult and Developmental Age “Gaetano Barresi”, University of Messina, c/o AOU Policlinico G. Martino, Via C. Valeria Gazzi, 98125 Messina, Italy
3
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, c/o AOU Policlinico G. Martino, Via C. Valeria Gazzi, 98125 Messina, Italy
*
Author to whom correspondence should be addressed.
Cancers 2020, 12(4), 1038; https://doi.org/10.3390/cancers12041038
Received: 13 April 2020 / Revised: 18 April 2020 / Accepted: 20 April 2020 / Published: 23 April 2020
Glioblastomas are aggressive cancers characterized by uncontrolled proliferation and inflammation. b-caryophyllene (BCP) is a cannabinoid receptor 2 (CB2) agonist that showed an important anti-inflammatory effect through the interaction of CB2 and peroxisome proliferator-activated receptor gamma (PPARg) receptors. BCP effects were investigated in an in vitro model of glioblastoma. U-373 and U87, derived from a human glioblastoma, and human glioma stem-like cells (GSCs) were treated with BCP at different doses and time-points. AM360, a specific CB2 antagonist, was added 2 h before BCP treatment. BCP showed a significant anti-proliferative effect, reducing cell viability, inhibiting cell cycle, and increasing apoptosis, as demonstrated by Tunel assay, caspase-3 and caspase -9 activation. In addition, the pro-apoptotic BAX expression was increased, whereas the anti-apoptotic Bcl-2 expression was reduced. Treatment with BCP decreased Beclin-1, LC3 and p62/SQSTM1 expression, indicating a possible switch of autophagy to apoptosis. BCP’s anti-inflammatory effect was demonstrated by NF-κB reduction, PPARg activation and TNF-a decrease; BCP significantly reduced Jun N-Terminal Kinase (JNK) expression as a consequence of TNF-α inhibition. AM360 abrogated BCP effects, thus demonstrating the BCP mechanism of action through the CB2 receptor. These findings let us hypothesize that BCP may act as a tumor suppressor in glioblastoma, acting on CB2 receptor and modulating JNK. View Full-Text
Keywords: glioblastoma; β-caryophyllene; CB2 receptor; apoptosis; inflammation glioblastoma; β-caryophyllene; CB2 receptor; apoptosis; inflammation
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MDPI and ACS Style

Irrera, N.; D’Ascola, A.; Pallio, G.; Bitto, A.; Mannino, F.; Arcoraci, V.; Rottura, M.; Ieni, A.; Minutoli, L.; Metro, D.; Vaccaro, M.; Altavilla, D.; Squadrito, F. β-Caryophyllene Inhibits Cell Proliferation through a Direct Modulation of CB2 Receptors in Glioblastoma Cells. Cancers 2020, 12, 1038. https://doi.org/10.3390/cancers12041038

AMA Style

Irrera N, D’Ascola A, Pallio G, Bitto A, Mannino F, Arcoraci V, Rottura M, Ieni A, Minutoli L, Metro D, Vaccaro M, Altavilla D, Squadrito F. β-Caryophyllene Inhibits Cell Proliferation through a Direct Modulation of CB2 Receptors in Glioblastoma Cells. Cancers. 2020; 12(4):1038. https://doi.org/10.3390/cancers12041038

Chicago/Turabian Style

Irrera, Natasha; D’Ascola, Angela; Pallio, Giovanni; Bitto, Alessandra; Mannino, Federica; Arcoraci, Vincenzo; Rottura, Michelangelo; Ieni, Antonio; Minutoli, Letteria; Metro, Daniela; Vaccaro, Mario; Altavilla, Domenica; Squadrito, Francesco. 2020. "β-Caryophyllene Inhibits Cell Proliferation through a Direct Modulation of CB2 Receptors in Glioblastoma Cells" Cancers 12, no. 4: 1038. https://doi.org/10.3390/cancers12041038

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