Cannabinoids inhibit peptidoglycan-induced phosphorylation of NF-κB and cell growth in U87MG human malignant glioma cells
Search this article
Description
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.
Journal
-
- Oncology Reports
-
Oncology Reports 28 (4), 1176-1170, 2012-10-01
Spandidos Publications
- Tweet
Keywords
- Morpholines
- Antineoplastic Agents
- Arachidonic Acids
- Peptidoglycan
- Naphthalenes
- Glycerides
- Central Nervous System Neoplasms
- Receptor, Cannabinoid, CB2
- Receptor, Cannabinoid, CB1
- Cell Line, Tumor
- Humans
- Phosphorylation
- Cell Proliferation
- Dose-Response Relationship, Drug
- Cannabinoids
- NF-kappa B
- Glioma
- Benzoxazines
- Pyrazoles
- Drug Screening Assays, Antitumor
- Endocannabinoids
Details 詳細情報について
-
- CRID
- 1050282810927673088
-
- NII Article ID
- 120005285923
-
- NII Book ID
- AA11016405
-
- ISSN
- 1021335X
- 17912431
-
- HANDLE
- 2297/34706
-
- PubMed
- 22842590
-
- Text Lang
- en
-
- Article Type
- journal article
-
- Data Source
-
- IRDB
- Crossref
- CiNii Articles
- KAKEN
- OpenAIRE
