ArticleOncotarget2014
FAAH inhibition enhances anandamide mediated anti-tumorigenic effects in non-small cell lung cancer by downregulating the EGF/EGFR pathway.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- ACPA decreases non-small cell lung cancer line growth through Akt/PI3K and JNK pathways in vitro.Cell death & disease · 2021Trial
- Cannabis in cancer: a review of therapeutic potential, clinical and preclinical status, and legislation.Archives of pharmacal research · 2026Review
- IGFBP1 is One of 10 Metabolic Factors Predicting Recurrence Free Survival in Gastric Cancer and Promotes Cancer Progression via ZFX-IGFBP1 Axis.OncoTargets and therapy · 2025Article
- Cannabidiol promotes apoptosis and downregulation of oncogenic factors.bioRxiv : the preprint server for biology · 2024Article
- A Novel Non-Psychoactive Fatty Acid from a Marine Snail,Molecules (Basel, Switzerland) · 2024Article
- Emerging Lipid Targets in Glioblastoma.Cancers · 2024Review
- Lipid metabolism-derived FAAH is a sensitive marker for the prognosis and immunotherapy of osteosarcoma patients.Heliyon · 2024Article
- Targeting Fatty Acid Amide Hydrolase Counteracts the Epithelial-to-Mesenchymal Transition in Keratinocyte-Derived Tumors.International journal of molecular sciences · 2023Article
- FAAH inhibition ameliorates breast cancer in a murine model.Oncotarget · 2023Article
- Article
- Inhibition of Fatty Acid Amide Hydrolase (FAAH) Regulates NF-kb Pathways Reducing Bleomycin-Induced Chronic Lung Inflammation and Pulmonary Fibrosis.International journal of molecular sciences · 2023Article
- Cannabinoids as Prospective Anti-Cancer Drugs: Mechanism of Action in Healthy and Cancer Cells.Advances in experimental medicine and biology · 2023Article
- N-linoleyltyrosine resisted the growth of non-small cell lung cancer cells via the regulation of CBFrontiers in pharmacology · 2023Article
- Molecular Basis for Non-Covalent, Non-Competitive FAAH Inhibition.International journal of molecular sciences · 2022Article
- Cannabinoid receptor 2 expression in early-stage non-small cell lung cancers identifies patients with good prognosis and longer survival.Translational lung cancer research · 2022Article
- Improved Therapeutic Efficacy of CBD with Good Tolerance in the Treatment of Breast Cancer through Nanoencapsulation and in Combination with 20(S)-Protopanaxadiol (PPD).Pharmaceutics · 2022Article
- Fatty Acid Amide Hydrolase (FAAH) Inhibition Plays a Key Role in Counteracting Acute Lung Injury.International journal of molecular sciences · 2022Article
- Endocannabinoid System and Tumour Microenvironment: New Intertwined Connections for Anticancer Approaches.Cells · 2021Review
- Review
- Molecular Mechanism of Cannabinoids in Cancer Progression.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The endocannabinoid anandamide (AEA), a neurotransmitter was shown to have anti-cancer effects. Fatty acid amide hydrolase (FAAH) metabolizes AEA and decreases its anti-tumorigenic activity. In this study, we have analyzed the role of FAAH inhibition in non-small cell lung cancer (NSCLC). We have shown that FAAH and CB1 receptor which is activated by AEA are expressed in lung adenocarcinoma patient samples and NSCLC cell lines A549 and H460. Since the synthetic analogue of anandamide (Met-F-AEA) did not possess significant anti-tumorigenic effects, we used Met-F-AEA in combination with FAAH inhibitor URB597 which significantly reduced EGF (epidermal growth factor)-induced proliferative and chemotactic activities in vitro when compared to anti-tumorigenic activity of Met-F-AEA alone. Further analysis of signaling mechanisms revealed that Met-F-AEA in combination with URB597 inhibits activation of EGFR and its downstream signaling ERK, AKT and NF-kB. In addition, it inhibited MMP2 secretion and stress fiber formation. We have also shown that the Met-F-AEA in combination with URB597 induces G0/G1 cell cycle arrest by downregulating cyclin D1 and CDK4 expressions, ultimately leading to apoptosis via activation of caspase-9 and PARP. Furthermore, the combination treatment inhibited tumor growth in a xenograft nude mouse model system. Tumors derived from Met-F-AEA and URB597 combination treated mice showed reduced EGFR, AKT and ERK activation and MMP2/MMP9 expressions when compared to Met-F-AEA or URB597 alone. Taken together, these data suggest in EGFR overexpressing NSCLC that the combination of Met-F-AEA with FAAH inhibitor resulted in superior therapeutic response compared to individual compound activity alone.
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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.