ArticleHepatology (Baltimore, Md.)2015
Cannabinoid receptor 1 promotes hepatocellular carcinoma initiation and progression through multiple mechanisms.
Article in Hepatology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 96 citations in OpenAlex.
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- Molecular Crosstalk and Therapeutic Synergy: Tyrosine Kinase Inhibitors and Cannabidiol in Oral Cancer Treatment.Current issues in molecular biology · 2025Review
- Cannabidiol (CBD) as a potential therapeutic agent for liver cancer: a comprehensive review of current evidence.Cancer cell international · 2025Review
- Cannabinoid-2 receptor depletion promotes non-alcoholic fatty liver disease in mice via disturbing gut microbiota and tryptophan metabolism.Acta pharmacologica Sinica · 2025Article
- CBD promotes antitumor activity by modulating tumor immune microenvironment in HPV associated head and neck squamous cell carcinoma.Frontiers in immunology · 2025Article
- Analysis and experimental validation of the innate immune gene PSMD1 in liver hepatocellular carcinoma and pan-cancer.Heliyon · 2023Article
- Cannabis- and Substance-Related Carcinogenesis in Europe: A Lagged Causal Inferential Panel Regression Study.Journal of xenobiotics · 2023Article
- The endocannabinoid system promotes hepatocyte progenitor cell proliferation and maturation by modulating cellular energetics.Cell death discovery · 2023Article
- Cannabinoids as Prospective Anti-Cancer Drugs: Mechanism of Action in Healthy and Cancer Cells.Advances in experimental medicine and biology · 2023Article
- Perturbation of 3D nuclear architecture, epigenomic aging and dysregulation, and cannabinoid synaptopathy reconfigures conceptualization of cannabinoid pathophysiology: part 2-Metabolome, immunome, synaptome.Frontiers in psychiatry · 2023Review
- Article
- Perturbation of 3D nuclear architecture, epigenomic dysregulation and aging, and cannabinoid synaptopathy reconfigures conceptualization of cannabinoid pathophysiology: part 1-aging and epigenomics.Frontiers in psychiatry · 2023Review
- Cannabinoids orchestrate cross-talk between cancer cells and endothelial cells in colorectal cancer.Cancer gene therapy · 2022Article
- LncRNA XIST accelerates burn wound healing by promoting M2 macrophage polarization through targeting IL-33 via miR-19b.Cell death discovery · 2022Article
- Geotemporospatial and causal inferential epidemiological overview and survey of USA cannabis, cannabidiol and cannabinoid genotoxicity expressed in cancer incidence 2003-2017: part 1 - continuous bivariate analysis.Archives of public health = Archives belges de sante publique · 2022Article
- Medical Cannabis in Pediatric Oncology: Friend or Foe?Pharmaceuticals (Basel, Switzerland) · 2022Review
- Therapeutic and prognostic potential of GPCRs in prostate cancer from multi-omics landscape.Frontiers in pharmacology · 2022Article
- Cannabinoid receptors promote chronic intermittent hypoxia-induced breast cancer metastasis via IGF-1R/AKT/GSK-3β.Molecular therapy oncolytics · 2021Article
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11 authors at 3 institutions in 1 country.
Funding
Abstract
unlabelledHepatocellular carcinoma (HCC) has high mortality and no adequate treatment. Endocannabinoids interact with hepatic cannabinoid 1 receptors (CB1Rs) to promote hepatocyte proliferation in liver regeneration by inducing cell cycle proteins involved in mitotic progression, including Forkhead Box M1. Because this protein is highly expressed in HCC and contributes to its genesis and progression, we analyzed the involvement of the endocannabinoid/CB1R system in murine and human HCC. Postnatal diethylnitrosamine treatment induced HCC within 8 months in wild-type mice but fewer and smaller tumors in CB1R(-/-) mice or in wild-type mice treated with the peripheral CB1R antagonist JD5037, as monitored in vivo by serial magnetic resonance imaging. Genome-wide transcriptome analysis revealed CB1R-dependent, tumor-induced up-regulation of the hepatic expression of CB1R, its endogenous ligand anandamide, and a number of tumor-promoting genes, including the GRB2 interactome as well as Forkhead Box M1 and its downstream target, the tryptophan-catalyzing enzyme indoleamine 2,3-dioxygenase. Increased indoleamine 2,3-dioxygenase activity and consequent induction of immunosuppressive T-regulatory cells in tumor tissue promote immune tolerance.
conclusionThe endocannabinoid/CB1R system is up-regulated in chemically induced HCC, resulting in the induction of various tumor-promoting genes, including indoleamine 2,3-dioxygenase; and attenuation of these changes by blockade or genetic ablation of CB1R suppresses the growth of HCC and highlights the therapeutic potential of peripheral CB1R blockade.
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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.