The Effect of Cannabidiol on the Viability and Anticancer Properties of Human NK Cells: Consequences for Therapies
- 1Laboratory of Immunology and Ionic Transport Regulation, Biomedical Research Centre, University of Colima, Av. 25 de Julio #965, Villas de San Sebastián, Colima 28045, Mexico
- 2Laboratory of Cancer Pathophysiology, University Center for Biomedical Research, University of Colima, Colima 28045, Mexico
- 3Secretariat of Science, Humanities, Technology and Innovation (SECIHTI), Researchers for Mexico Program, Mexico City 03940, Mexico
Abstract
The palliative and anti-cancer properties of CBD are attracting increasing attention. We have examined the dose-dependent effects of CBD on the viability and antitumor properties of human NK cells. CBD killed NK cells with an apparent IC50 of 77 μM at 24–48 h of incubation. Concentrations up to 10 μM caused neither cell death nor a significant decrease in metabolic activity, whereas concentrations above 30 μM provoked cell death. The antagonist of CB1 partly reverted CBD cytotoxicity, whereas the antagonist of CB2 was inefficient. Cyclosporin A (CsA), an inhibitor of the mitochondrial permeability transition pore, mPTP, strongly suppressed the CBD cytotoxicity. CBD produced the CsA-sensitive depolarization of mitochondrial membrane potential in leukemic Jurkat cells, with a lesser effect on NK cells. The cytotoxicity of NK cells against Jurkat cells was evaluated in a 1:1 co-culture. Different donors displayed greatly variable NK cells’ degranulation, which was unaffected by a pre-treatment with up to 25 μM of CBD. NK cells from half of the tested donors displayed maximal cytotoxicity against target cells upon pretreatment with up to 25 μM of CBD, whereas in others, NK cytotoxicity decreased by 60%. Therefore, the appropriateness of including CBD in anticancer treatment should be carefully assessed based on the concentrations expected for palliative or antitumor effects.
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BibTeX
@article{gutierreziniguez2026effect,
title = {{The Effect of Cannabidiol on the Viability and Anticancer Properties of Human NK Cells: Consequences for Therapies}},
author = {Cecilia Gutiérrez-Iñiguez and Miguel Olivas-Aguirre and Igor Pottosin and Oxana Dobrovinskaya},
journal = {Biomolecules},
year = {2026},
month = oct,
doi = {10.3390/biom16101491},
url = {https://www.mdpi.com/2218-273X/16/10/1491},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The Effect of Cannabidiol on the Viability and Anticancer Properties of Human NK Cells: Consequences for Therapies
AU - Cecilia Gutiérrez-Iñiguez
AU - Miguel Olivas-Aguirre
AU - Igor Pottosin
AU - Oxana Dobrovinskaya
PY - 2026
DA - 2026/10/01
JO - Biomolecules
DO - 10.3390/biom16101491
UR - https://www.mdpi.com/2218-273X/16/10/1491
AB - The palliative and anti-cancer properties of CBD are attracting increasing attention. We have examined the dose-dependent effects of CBD on the viability and antitumor properties of human NK cells. CBD killed NK cells with an apparent IC50 of 77 μM at 24–48 h of incubation. Concentrations up to 10 μM caused neither cell death nor a significant decrease in metabolic activity, whereas concentrations above 30 μM provoked cell death. The antagonist of CB1 partly reverted CBD cytotoxicity, whereas the antagonist of CB2 was inefficient. Cyclosporin A (CsA), an inhibitor of the mitochondrial permeability transition pore, mPTP, strongly suppressed the CBD cytotoxicity. CBD produced the CsA-sensitive depolarization of mitochondrial membrane potential in leukemic Jurkat cells, with a lesser effect on NK cells. The cytotoxicity of NK cells against Jurkat cells was evaluated in a 1:1 co-culture. Different donors displayed greatly variable NK cells’ degranulation, which was unaffected by a pre-treatment with up to 25 μM of CBD. NK cells from half of the tested donors displayed maximal cytotoxicity against target cells upon pretreatment with up to 25 μM of CBD, whereas in others, NK cytotoxicity decreased by 60%. Therefore, the appropriateness of including CBD in anticancer treatment should be carefully assessed based on the concentrations expected for palliative or antitumor effects.
SN - 2218-273X
ER -