ArticleCell death & disease2013
Involvement of PPARγ in the antitumoral action of cannabinoids on hepatocellular carcinoma.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Cys-loop receptors on cannabinoids: All high?Frontiers in physiology · 2022Pooled it
- Cannabinoids in Cancer: Molecular Mechanisms of Tumor Cell Death and Translational Opportunities.Biomolecules · 2026Review
- ΔJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Antitumor Activity of Cannabinoids and Their Interaction with Chemotherapy: A Systematic Review and Meta-Analysis of Preclinical Evidence.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Differential Regulatory Effects of Cannabinoids and Vitamin E Analogs on Cellular Lipid Homeostasis and Inflammation in Human Macrophages.Antioxidants (Basel, Switzerland) · 2026Article
- Multiple binding modes underlieFrontiers in bioinformatics · 2026Article
- Cannabinoids in oncology: pharmacology, clinical applications, and translational perspectives.Frontiers in pharmacology · 2026Review
- Durable complete response of advanced hepatocellular carcinoma using cannabis oil: a report of two cases.Journal of cannabis research · 2025Article
- Targeting bladder cancer: Potent anti-cancer effects of cannabichromene and delta-9-tetrahydrocannabinol-richAsian journal of urology · 2025Article
- Distinct Adipocyte Responses to ΔInternational journal of molecular sciences · 2025Article
- Pharmacological advances in cannabinoid-based therapies for pancreatic cancer: preclinical efficacy of CCL-106 and its epimers.ESMO gastrointestinal oncology · 2025Article
- Cannabidiol (CBD) as a potential therapeutic agent for liver cancer: a comprehensive review of current evidence.Cancer cell international · 2025Review
- Impact of cannabinoids on cancer outcomes in patients receiving immune checkpoint inhibitor immunotherapy.Frontiers in immunology · 2025Review
- PPARα and PPARγ are expressed in midbrain dopamine neurons and modulate dopamine- and cannabinoid-mediated behavior in mice.Molecular psychiatry · 2023Article
- Decoding the Postulated Entourage Effect of MedicinalBiomedicines · 2023Review
- NLRC5 affects diet-induced adiposity in female mice and co-regulates peroxisome proliferator-activated receptor PPARγ target genes.iScience · 2023Article
- PPARα and PPARγ are expressed in midbrain dopamine neurons and modulate dopamine- and cannabinoid-mediated behavior in mice.Research square · 2023Article
- Cannabidiol regulates apoptosis and autophagy in inflammation and cancer: A review.Frontiers in pharmacology · 2023Review
- The endocannabinoid system and breathing.Frontiers in neuroscience · 2023Review
- Cannabinoids as Prospective Anti-Cancer Drugs: Mechanism of Action in Healthy and Cancer Cells.Advances in experimental medicine and biology · 2023Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cannabinoids exert antiproliferative effects in a wide range of tumoral cells, including hepatocellular carcinoma (HCC) cells. In this study, we examined whether the PPARγ-activated pathway contributed to the antitumor effect of two cannabinoids, Δ9-tetrahydrocannabinol (THC) and JWH-015, against HepG2 and HUH-7 HCC cells. Both cannabinoids increased the activity and intracellular level of PPARγ mRNA and protein, which was abolished by the PPARγ inhibitor GW9662. Moreover, genetic ablation with small interfering RNA (siRNA), as well as pharmacological inhibition of PPARγ decreased the cannabinoid-induced cell death and apoptosis. Likewise, GW9662 totally blocked the antitumoral action of cannabinoids in xenograft-induced HCC tumors in mice. In addition, PPARγ knockdown with siRNA caused accumulation of the autophagy markers LC3-II and p62, suggesting that PPARγ is necessary for the autophagy flux promoted by cannabinoids. Interestingly, downregulation of the endoplasmic reticulum stress-related protein tribbles homolog 3 (TRIB3) markedly reduced PPARγ expression and induced p62 accumulation, which was counteracted by overexpression of PPARγ in TRIB3-knocked down cells. Taken together, we demonstrate for the first time that the antiproliferative action of the cannabinoids THC and JWH-015 on HCC, in vitro and in vivo, are modulated by upregulation of PPARγ-dependent pathways.
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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.