R(+)-Methanandamide Elicits a Cyclooxygenase-2-Dependent Mitochondrial Apoptosis Signaling Pathway in Human Neuroglioma Cells

@article{Eichele2005RMethanandamideEA,
  title={R(+)-Methanandamide Elicits a Cyclooxygenase-2-Dependent Mitochondrial Apoptosis Signaling Pathway in Human Neuroglioma Cells},
  author={K. Eichele and U. Weinzierl and R. Ramer and K. Brune and B. Hinz},
  journal={Pharmaceutical Research},
  year={2005},
  volume={23},
  pages={90-94}
}
PurposeCannabinoids have been associated with tumor regression and apoptosis of cancer cells. Recently, we have shown that R(+)-methanandamide (R(+)-MA) induces apoptosis of H4 human neuroglioma cells via a mechanism involving de novo expression of the cyclooxygenase-2 (COX-2) enzyme. The present study investigated a possible involvement of a mitochondrial-driven pathway in this process.MethodsCell death was determined by the WST-1 cell viability test, and changes in apoptotic parameters [i.e… Expand
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References

SHOWING 1-10 OF 41 REFERENCES
Up-Regulation of Cyclooxygenase-2 Expression Is Involved in R(+)-Methanandamide-Induced Apoptotic Death of Human Neuroglioma Cells
TLDR
COX-2 is defined as a hitherto unknown target by which a cannabinoid induces apoptotic death of glioma cells and the data show that pharmacological concentrations of celecoxib may interfere with the proapoptotic action of R(+)-MA and anandamide, suggesting that cotreatment with COx-2 inhibitors could diminishglioma regression induced by these compounds. Expand
Ceramide is involved in r(+)-methanandamide-induced cyclooxygenase-2 expression in human neuroglioma cells.
TLDR
Results demonstrate that R(+)-MA induces COX-2 expression in human neuroglioma cells via synthesis of ceramide and subsequent activation of p38 and p42/44 MAPK pathways. Expand
Prostaglandin D2 and J2 induce apoptosis in human leukemia cells via activation of the caspase 3 cascade and production of reactive oxygen species
TLDR
The presence of prostaglandins (PGs) has been demonstrated in the processes of carcinogenesis and inflammation and a differential apoptotic effect of PGs through ROS production, followed by activation of the caspase 3 cascade, was demonstrated. Expand
R(+)-methanandamide induces cyclooxygenase-2 expression in human neuroglioma cells via a non-cannabinoid receptor-mediated mechanism.
TLDR
It is demonstrated that R(+)-methanandamide induces COX-2 expression in human neuroglioma cells via a cannabinoid receptor-independent mechanism involving activation of the MAPK pathway. Expand
De novo-synthesized ceramide is involved in cannabinoid-induced apoptosis.
TLDR
De novo-synthesized ceramide is involved in cannabinoid-induced apoptosis of glioma cells, and pharmacological inhibition of ceramide synthesis de novo prevented the stimulation of extracellular-signal-regulated kinase and the inhibition of protein kinase B triggered by cannabinoids. Expand
Inhibition of paclitaxel-induced apoptosis by the specific COX-2 inhibitor, NS398, in epithelial ovarian cancer cells.
TLDR
Combining COX-2 inhibitors and paclitaxel does not have an additive or synergistic tumoricidal effect and, on the contrary, NS398 treatment markedly inhibited the apoptotic effects of pac litaxel in each of these two EOC cell lines. Expand
Microtubule-interfering Agents Stimulate the Transcription of Cyclooxygenase-2
TLDR
Microtubule- or actin-interfering agents stimulated MAPK signaling and activator protein-1 activity, which led, in turn, to induction of COX-2 gene expression via the cyclic AMP response element site in the COx-2 promoter. Expand
Binding, degradation and apoptotic activity of stearoylethanolamide in rat C6 glioma cells.
TLDR
It seems noteworthy that degradation and pro-apoptotic activity of SEA are regulated by NO in a way opposite to that reported for AEA, suggesting that this compound also has an 'entourage' effect. Expand
Malignant Transformation and Antineoplastic Actions of Nonsteroidal Antiinflammatory Drugs (Nsaids) on Cyclooxygenase-Null Embryo Fibroblasts
TLDR
The findings with cyclooxygenase knockout cells confirm recent reports that some of the antiproliferative and antineoplastic effects of NSAIDs are independent of the inhibition of either COX-1 orCOX-2, and suggest that the involvement of the cyclo oxygengenases in tumorigenesis may occur at later steps. Expand
Induction of G0/G1 cell cycle arrest in ovarian carcinoma cells by the anti-inflammatory drug NS-398, but not by COX-2-specific RNA interference
TLDR
The experiments suggest that NS-398 reduced cell proliferation in ovarian carcinoma cells by induction of G0/G1 cell cycle arrest independent of COX-2 inhibition, and shows that specific inhibition ofCOX isoforms by RNAi could be used to dissociate effects of NSAIDs. Expand
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