Abstract
Cannabinoids recently have been shown to control the cell survival/death decision. Thus, cannabinoids induce growth arrest or apoptosis in a number of transformed neural and non-neural cells in culture. In addition, cannabinoid administration induces regression of malignant gliomas in rodents by a mechanism that may involve sustained ceramide generation and extracellular signal-regulated kinase activation. In contrast, most of the experimental evidence indicates that cannabinoids may protect normal neurons from toxic insults, such as glutamatergic overstimulation, ischaemia, and oxidative damage. Regarding immune cells, low doses of cannabinoids may enhance proliferation, whereas high doses of cannabinoids usually induce growth arrest or apoptosis. The potential therapeutic applications of these findings are discussed.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antineoplastic Agents / therapeutic use
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Cannabinoid Receptor Modulators
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Cannabinoids / pharmacology*
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Cannabinoids / therapeutic use
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Cell Death / drug effects
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Cell Division / drug effects
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Cell Survival / drug effects
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Cell Transformation, Neoplastic
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Fatty Acids, Unsaturated / metabolism
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Humans
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Immune System / cytology
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Immune System / drug effects
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Immunosuppressive Agents / pharmacology
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Multiple Sclerosis / drug therapy
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Neurons / cytology
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Neurons / drug effects
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Neuroprotective Agents / therapeutic use
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Receptors, Cannabinoid
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Receptors, Drug / drug effects
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Receptors, Drug / physiology
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Signal Transduction
Substances
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Antineoplastic Agents
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Cannabinoid Receptor Modulators
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Cannabinoids
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Fatty Acids, Unsaturated
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Immunosuppressive Agents
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Neuroprotective Agents
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Receptors, Cannabinoid
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Receptors, Drug