Chapter title |
Cannabinoid signaling in glioma cells.
|
---|---|
Chapter number | 11 |
Book title |
Glioma Signaling
|
Published in |
Advances in experimental medicine and biology, July 2012
|
DOI | 10.1007/978-94-007-4719-7_11 |
Pubmed ID | |
Book ISBNs |
978-9-40-074718-0, 978-9-40-074719-7
|
Authors |
Aleksandra Ellert-Miklaszewska, Iwona Ciechomska, Bozena Kaminska, Ellert-Miklaszewska, Aleksandra, Ciechomska, Iwona, Kaminska, Bozena |
Editors |
Jolanta Barańska |
Abstract |
Cannabinoids are a group of structurally heterogeneous but pharmacologically related compounds, including plant-derived cannabinoids, synthetic substances and endogenous cannabinoids, such as anandamide and 2-arachidonoylglycerol. Cannabinoids elicit a wide range of central and peripheral effects mostly mediated through cannabinoid receptors. There are two types of specific G(i/o)-protein-coupled receptors cloned so far, called CB1 and CB2, although an existence of additional cannabinoid-binding receptors has been suggested. CB1 and CB2 differ in their predicted amino acid sequence, tissue distribution, physiological role and signaling mechanisms. Significant alterations of a balance in the cannabinoid system between the levels of endogenous ligands and their receptors occur during malignant transformation in various types of cancer, including gliomas. Cannabinoids exert anti-proliferative action in tumor cells. Induction of cell death by cannabinoid treatment relies on the generation of a pro-apoptotic sphingolipid ceramide and disruption of signaling pathways crucial for regulation of cellular proliferation, differentiation or apoptosis. Increased ceramide levels lead also to ER-stress and autophagy in drug-treated glioblastoma cells. |
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Mendeley readers
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Immunology and Microbiology | 2 | 4% |
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