Cannabinoids inhibit peptidoglycan-induced phosphorylation of NF-κB and cell growth in U87MG human malignant glioma cells

Echigo,Ryosuke; Sugimoto,Naotoshi; Yachie,Akihiro; Ohno-Shosaku,Takako

doi:10.3892/or.2012.1937

October 2012 Volume 28 Issue 4

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October 2012 Volume 28 Issue 4

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Article

Cannabinoids inhibit peptidoglycan-induced phosphorylation of NF-κB and cell growth in U87MG human malignant glioma cells

Authors:
- Ryosuke Echigo
- Naotoshi Sugimoto
- Akihiro Yachie
- Takako Ohno-Shosaku
View Affiliations / Copyright

Affiliations: Department of Impairment Study, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan, Department of Physiology, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan, Department of Pediatrics, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan
Pages: 1176-1180
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Published online on: July 26, 2012

https://doi.org/10.3892/or.2012.1937
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Abstract

Nuclear factor (NF)-κB is the key transcription factor involved in the inflammatory responses, and its activation aggravates tumors. Peptidoglycan (PGN), a main cell wall component of Gram-positive bacteria, stimulates Toll-like receptor 2 (TLR-2) and activates a number of inflammatory pathways, including NF-κB. Cannabinoids have been reported to exert anti-inflammatory and antitumor effects. The mechanisms underlying these actions, however, are largely unknown. The purpose of this study was to investigate whether cannabinoids can suppress the PGN-induced activation of NF-κB and cell growth via cannabinoid receptors in U87MG human malignant glioma cells. PGN treatment induced the phosphorylation of NF-κB and cell proliferation in a concentration-dependent manner. The main endocannabinoid, 2-arachidonoylglycerol, prevented the PGN-induced phosphorylation of NF-κB, which was reversed by the CB1 cannabinoid receptor antagonist, AM281. The synthetic cannabinoid, WIN55,212-2, abolished the PGN-activated cell growth, and this effect was reversed by AM281. The preferential expression of CB1 rather than CB2 receptors in these cells was confirmed by reverse transcription-mediated polymerase chain reaction experiments and the observation that the WIN55,212-2-induced morphological changes were completely reversed by AM281 but not by the CB2 antagonist, AM630. Our finding that cannabinoids suppress the NF-κB inflammatory pathway and cell growth via CB1 receptors in glioma cells provides evidence for the therapeutic potential of targeting cannabinoid receptors for the treatment of inflammation-dependent tumor progression.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

Cannabinoids inhibit peptidoglycan-induced phosphorylation of NF-κB and cell growth in U87MG human malignant glioma cells

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