ArticleMolecular carcinogenesis2012
Arachidonoyl ethanolamide (AEA)-induced apoptosis is mediated by J-series prostaglandins and is enhanced by fatty acid amide hydrolase (FAAH) blockade.
Article in Molecular carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Interaction of endocannabinoid system and cyclooxygenase metabolites with fatty acid amide hydrolase and cyclooxygenase enzyme activities on contractile responses in rat vas deferens tissue.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Targeting Fatty Acid Amide Hydrolase Counteracts the Epithelial-to-Mesenchymal Transition in Keratinocyte-Derived Tumors.International journal of molecular sciences · 2023Article
- N-linoleyltyrosine resisted the growth of non-small cell lung cancer cells via the regulation of CBFrontiers in pharmacology · 2023Article
- Cannabidiol regulates apoptosis and autophagy in inflammation and cancer: A review.Frontiers in pharmacology · 2023Review
- Calcium signaling induced by 15-deoxy-prostamide-J2 promotes cell death by activating PERK, IP3R, and the mitochondrial permeability transition pore.Oncotarget · 2022Article
- Influence of Inhibition of COX-2-Dependent Lipid Metabolism on Regulation of UVB-Induced Keratinocytes Apoptosis by Cannabinoids.Biomolecules · 2022Article
- Impact of Cannabinoid Compounds on Skin Cancer.Cancers · 2022Review
- Involvement of Metabolic Lipid Mediators in the Regulation of Apoptosis.Biomolecules · 2020Review
- Cannabinoids in the Pathophysiology of Skin Inflammation.Molecules (Basel, Switzerland) · 2020Review
- Cannabinoids Modulate Neuronal Activity and Cancer by CB1 and CB2 Receptor-Independent Mechanisms.Frontiers in pharmacology · 2017Review
- Lovastatin lactone elicits human lung cancer cell apoptosis via a COX-2/PPARγ-dependent pathway.Oncotarget · 2016Article
- Induction but not inhibition of COX-2 confers human lung cancer cell apoptosis by celecoxib.Journal of lipid research · 2013Article
- Receptor-dependent and receptor-independent endocannabinoid signaling: a therapeutic target for regulation of cancer growth.Life sciences · 2013Review
- The Endocannabinoid System in the Postimplantation Period: A Role during Decidualization and Placentation.International journal of endocrinology · 2013Review
- The endocannabinoid system in prostate cancer.Nature reviews. Urology · 2011Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The endocannabinoid arachidonoyl ethanolamide (AEA) is a potent inducer of tumor cell apoptosis however its mechanism of cytotoxicity is unclear. A previous report from our laboratory showed that AEA induced cell death in a cyclooxygenase-2 (COX-2)-dependent manner and in this report our data indicate that AEA-induced apoptosis is mediated by COX-2 metabolic products of the J-series. In experiments conducted with JWF2 keratinocytes which over-express COX-2, AEA caused a concentration-regulated increase in J-series prostaglandin production and apoptosis. Similarly, cell treatment with exogenously added J-series prostaglandins (15-deoxy, Δ(12,14) PGJ(2) and PGJ(2)) induced apoptosis. AEA-induced apoptosis was inhibited by the antioxidant, N-acetyl cysteine, indicating that reactive oxygen species generation was required for apoptosis. Using antagonists of cannabinoid receptor 1, cannabinoid receptor 2, or transient receptor potential cation channel, subfamily V, member 1, it was observed that cannabinoid receptor inhibition did not block AEA-mediated cell death. In contrast, an inhibitor of fatty acid amide hydrolase (FAAH) potentiated AEA-induced J-series PG synthesis and apoptosis. These results suggest that the metabolism of AEA to J-series PGs regulates the induction of apoptosis in cells with elevated COX-2 levels. Our data further indicate that the proapoptotic activity of AEA can be enhanced by combining it with an inhibitor of FAAH. As such, AEA may be an effective agent to eliminate tumor cells that over-express COX-2.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.