A study published in Scientific Reports found that cannabidiol (CBD) disrupts lipid metabolism and induces apoptosis in ovarian cancer cells through cannabinoid receptor type 1 (CB1R)-mediated endoplasmic reticulum (ER) stress.
Researchers examined how CBD affects lipid metabolic pathways in ovarian cancer cells, given the role of metabolic reprogramming in tumor survival. The study found that CBD significantly inhibited ovarian cancer cell proliferation, reduced fatty acid levels, and suppressed the expression of genes involved in fatty acid uptake and synthesis.
Further analysis using RNA sequencing and real-time RT-PCR revealed that CBD activated ER stress pathways, leading to apoptosis. When researchers supplemented cells with unsaturated fatty acids or blocked CB1R, ER stress, or reactive oxygen species (ROS) signals, they observed a significant reduction in CBD-induced apoptosis, G0-G1 phase cell cycle arrest, and mitochondrial dysfunction.
These findings suggest that CBD’s ability to interfere with lipid metabolism and trigger ER stress-related apoptosis could contribute to its potential as an anti-ovarian cancer treatment.
The study’s full abstract can be found below:
Abstract
Ovarian cancer (OC) is the most deadly gynecological tumor. OC cells utilize cellular metabolic reprogramming to gain a survival advantage, particularly through aberrant lipid metabolic process. As the primary ingredient in exogenous cannabinoids, cannabidiol (CBD) has been confirmed to exhibit antitumor activity in preclinical studies. However, it is still unclear whether CBD can disrupt fatty acid metabolism and induce apoptosis in OC cells. In this study, we have demonstrated that CBD significantly inhibits the proliferation of OCs through a cannabinoid receptor type 1 (CB1R)-mediated manner. Fatty acid metabolic profiling and flow cytometry analysis revealed that CBD has the ability to decrease fatty acid levels and significantly suppress the transcription of genes involved in fatty acid uptake and synthesis in ES-2 cells. In addition, the analysis from RNA-seq and real-time RT-PCR revealed that CBD activated the endoplasmic reticulum (ER) stress pathway. Conversely, by supplementation with unsaturated fatty acid or blocking CB1R, ER stress or reactive oxygen species (ROS) signals with specific inhibitors could significantly relieve CBD induced, dose-dependent, ER stress associated apoptosis, G0-G1 phase arrest, and mitochondrial dysfunction. Taken collectively, these data indicate that CBD may disrupt lipid metabolism, and lead to ER stress-related apoptosis in OCs. Our findings may provide a theoretical mechanism for anti-ovarian cancer using CBD.
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