Category Archives: Cancer

Cannabidiol Inhibits Melanoma Progression by Regulating PPARγ-TET1 Complex-dependent LRASM1 Demethylation

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“Melanoma represents one of the most aggressive forms of skin cancers, with advanced metastatic stages largely managed through chemotherapy. However, current therapeutic strategies remain limited by drug resistance and systemic toxicity. Cannabidiol (CBD), the primary nonpsychoactive constituent of Cannabis sativa, has recently attracted attention for its anticancer properties across multiple tumor types.

OBJECTIVES

This study aimed to explore the antitumor efficacy of CBD in melanoma and elucidate its underlying molecular mechanisms, with the goal of identifying novel therapeutic strategies to overcome resistance and reduce adverse effects associated with conventional treatments.

METHODS

The antiproliferative and pro-apoptotic effects of CBD were assessed in vitro using MTS, EdU, Transwell invasion, and flow cytometry. In vivo efficacy was evaluated using a murine lung metastasis model. Potential CBD targets in melanoma were identified through network pharmacology and molecular docking, with a focus on peroxisome proliferator-activated receptor γ (PPARγ) and validation by western blotting and immunofluorescence. Integrated transcriptomic and genome-wide methylation analyses were performed to investigate epigenetic modifications induced by CBD. Co-immunoprecipitation and chromatin immunoprecipitation assays were employed to detect the interaction between PPARγ and ten-eleven translocation 1 (TET1), including their binding to promoter regions of downstream factors. Methylation-regulated target genes were further validated using qPCR and MeDIP PCR.

RESULTS

CBD significantly induced apoptosis and inhibited cell proliferation and invasion of melanoma cells in vitro, while reducing pulmonary metastasis in vivo. Pharmacological and molecular docking analyses, supported by protein-level validation, identified PPARγ as a critical mediator of CBD activity. Transcriptomic and methylation analyses revealed that CBD modulated global DNA methylation patterns, partly through the formation of a PPARγ-TET1 complex. This complex regulated the demethylation of leucine-rich repeat and sterile alpha motif-containing 1 (LRSAM1), a newly identified anticancer gene whose upregulation markedly enhanced melanoma cell apoptosis and suppressed proliferation.

CONCLUSIONS

CBD exhibited strong antitumor activity in melanoma by modulating the PPARγ–TET1 complex to induce demethylation of LRSAM1, thereby suppressing tumor progression. These findings identify CBD as a promising candidate for melanoma therapy.”

https://www.sciencedirect.com/science/article/abs/pii/S0944711326000127

“In summary, this study investigated molecular targets and mechanisms by which CBD suppresses melanoma progression, emphasizing its role in PPARγ activation and epigenetic regulation. These findings establish a mechanistic basis and provide candidate targets for future clinical application of CBD in melanoma treatment.”

“This study provides the first evidence that CBD inhibits melanoma progression by modulating gene methylation. The identification of LRSAM1 as a PPARγ-TET1-regulated tumor suppressor expands current understanding of epigenetic regulation in melanoma and highlights LRSAM1 as a viable therapeutic target.”

https://www.scilit.com/publications/50c9c0a6d08f7880cebb9c69a2c3fca7

Phytocannabinoids influence phospholipid metabolism of melanoma cells: Modulation of in vitro effects of the UVA irradiation

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“The high metastatic potential of melanoma and its poor prognosis in advanced stages motivate the search for innovative therapeutic approaches. Therefore, this study aimed to assess the effects of phytocannabinoids (cannabidiol-CBD, and cannabigerol-CBG) on the structure and function of the melanoma cell membrane, phospholipid metabolism, and the respective metabolites generated in ROS- and enzyme-dependent reactions.

Biochemical and physicochemical parameters were analyzed in melanoma cells (SK-MEL-5) cultured for 24 h with CBD (5 µM), CBG (1 µM), and their combination applied either alone or after UVA irradiation (365 nm) at a dose of 18 J/cm².

Phytocannabinoids have been shown to partially counteract changes in the levels of cell membrane components, including phospholipid polyunsaturated fatty acids (PUFAs) and sialic acid, consequently affecting surface charge density and lipid rafts, which may be a potential target for anticancer therapy. Furthermore, by changing the activity of lipolytic enzymes (PLA2/COX1/2/LOX-5), phytocannabinoids partially enhanced the UVA-induced decrease in free PUFAs. Consequently, the levels of lipid mediators, including endocannabinoids and eicosanoids, were altered.

The use of phytocannabinoids led to a significant increase in 2-AG levels, while the combined action of CBD/CBG reduced the levels of pro-inflammatory eicosanoids. UVA radiation increased the expression of G-protein-coupled receptors in melanoma cells (CB1/2/TRPV1/PPARγ), while the combined use of CBD/CBG reduced their expression.

Therefore, the results have shown that CBD and CBG modulate the metabolism of phospholipids and PUFAs by altering the functions of melanoma cell membranes, potentially offering options for the use of these phytocannabinoids in the integrative biomedicine treatment of melanoma.”

https://pubmed.ncbi.nlm.nih.gov/41529510

“Phytocannabinoids modulate endocannabinoid levels, supporting antitumor activity.”

“In summary, the results of this study indicate that phytocannabinoids (CBD and/or CBG) alter the functionality of melanoma cell membranes by modeling the structure and metabolism of phospholipids and free PUFAs, which may offer potential benefits in integrated melanoma therapy.”

https://www.sciencedirect.com/science/article/pii/S0753332226000351?via%3Dihub

Stability and Degradation-based Proteome Profiling Reveals Cannabidiol as a Promising CDC123-eIF2γ Inhibitor for Colorectal Cancer Therapy

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“Natural products (NPs) have long been foundational in drug discovery, offering unparalleled molecular diversity and complex mechanisms of action. However, identifying molecular targets for NPs remains a significant challenge.

This study introduces stability- and degradation-based proteome profiling (SDPP), which integrates orthogonal principles of thermal stability and degradation activity to enhance target identification precision and expand the NP target landscape, mediating dual regulation of protein stability: extracellularly through small-molecule-binding-induced thermodynamic stabilization and intracellularly via ligand-triggered proteolytic degradation.

Using SDPP, cannabidiol (CBD) is identified as a novel protein-protein interaction (PPI) inhibitor targeting the CDC123-eIF2γ complex, leading to sustained activation of the integrated stress response and apoptosis in colorectal cancer (CRC) cells.

Disruption of the CDC123-eIF2γ complex by CBD offers a selective therapeutic strategy for CRC. Importantly, CDC123 is recognized as an oncogenic driver in CRC, with elevated expression correlating with poor patient prognosis.

These findings establish SDPP as a robust framework for NP target identification and position CBD as a first-in-class natural PPI inhibitor with a promising therapeutic potential.”

https://pubmed.ncbi.nlm.nih.gov/41518300

https://pubs.acs.org/doi/10.1021/jacs.5c20040

Potential Anticancer Effect of Cannabis sativa L. Dichloromethane Extract Through Oxidative Stress-Related Pathways and the Inhibition of the Migration and Invasiveness of Human Breast Cancer Cells (MDA-MB-231 and MCF-7)

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“Breast cancer remains a leading cause of cancer-related morbidity and mortality globally, highlighting the urgent need for novel therapeutic strategies.

This study investigates the molecular mechanisms underlying the anti-proliferative potential of Cannabis sativa dichloromethane extract (C. sativa DCM) on oxidative stress, apoptosis, and invasion in human breast cancer cells.

Key biomarkers, such as antioxidant enzymes (Superoxide Dismutase (SOD) and Glutathione (GSH)), the transcription factor Nrf2, apoptotic proteins (p53, caspase-8 and 9), metalloproteinase (MMP-1 and MMP-9), and Transforming Growth Factor Beta (TGF-β) were examined. Cytotoxicity was assessed using an MTT assay in the MDA-MB-231 and MCF-7 breast cancer cell lines, with comparisons to normal skin fibroblasts (HS27). Oxidative stress biomarkers were quantified using enzymatic assays and ELISA kits, while apoptotic and anti-metastatic factors were determined by Western blotting.

Results demonstrated that C. sativa DCM extract induced significant cell death in a concentration-dependent manner, with IC50 values of 75.46 ± 0.132 μg/mL for MDA-MB-231 and 78.68 ± 0.50 μg/mL for MCF-7 cells. The extract decreased SOD and GSH levels while increasing p53 and caspase activity, confirming apoptosis activation. Additionally, C. sativa DCM inhibited migration and invasion by downregulating MMP-1, MMP-9, and TGF-β. The anti-proliferative potential of C. sativa DCM in breast cancer cells is mediated through a continuous biological pathway involving oxidative stress modulation, apoptotic signaling, and anti-invasive effects. Phytochemical analysis revealed terpenoids and steroids, including compounds like cannabidiol and tetrahydrocannabinol acid.

These findings suggest that C. sativa DCM extract holds potential as an anti-breast cancer therapeutic and warrants further preclinical and clinical investigations.”

https://pubmed.ncbi.nlm.nih.gov/41516029

“Cannabis sativa L., known in many slang languages as marijuana, bhang, ganja, for instance, is an herbaceous species originating from Central Asia and widely distributed around the world. It has been used as a source of fiber, food, oil, and for its multiple curative properties, including anti-parasitic, antipyretic, antibacterial, antitumor, vermifuge, dermatic, and pain-killing properties for centuries. Phytocannabinoids, derived from cannabis, have shown anti-cancer activity in cell lines”

“Based on these research findings, we concluded that C. sativa DCM extract possesses the potential to inhibit the proliferation of breast cancer cells (MCF-7 and MDA-MB-231), while exhibiting minimal cytotoxic effect on normal skin cells Hs27.”

“Given these conclusive findings, the presence of bioactive phytochemicals in C. sativa DCM can be considered as a potential source of anti-cancer agents.”

https://www.mdpi.com/1422-0067/27/1/152


Unlocking the potential: Cannabidiol (CBD) as a promising anti-tumor agent

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“Background: Cannabidiol (CBD), the primary non-psychoactive component of cannabis, is renowned for its antiepileptic, analgesic, and anti-inflammatory properties. Emerging evidence highlights its potential as an anti-tumor agent, yet significant heterogeneity in preclinical studies and an incomplete mechanistic understanding impede its clinical translation.

Purpose: This review aims to systematically evaluate the anti-tumor efficacy, underlying mechanisms, and safety profile of CBD, and to discuss the challenges and future directions for its application in oncology.

Study design: A systematic review.

Methods: We integrated recent high-quality research to assess CBD’s effects across various cancer types. The analysis encompassed its mechanisms in tumor cell biology and the tumor microenvironment (TME), a comparison of monotherapy versus combination therapy efficacy, its role in managing cancer-related symptoms, and its pharmacokinetic/pharmacodynamic properties. Advances in nano-based drug delivery systems were also reviewed.

Results: CBD demonstrates multi-target anti-tumor effects, including inhibiting proliferation, inducing apoptosis, suppressing metastasis, and remodeling the TME via immunomodulation. It exhibits broad-spectrum efficacy in vitro and in vivo, shows synergistic effects in combination therapy, and can alleviate cancer-related symptoms. Safety data indicate a favorable tolerability profile. However, current evidence relies predominantly on preclinical models.

Conclusion: CBD holds substantial promise as an anti-tumor agent. This review provides a theoretical foundation for its rational development. Future work should focus on validating these findings in clinical trials, optimizing targeted drug delivery systems, and establishing standardized treatment protocols.”

https://pubmed.ncbi.nlm.nih.gov/41494497

“CBD, a non-psychoactive phytocannabinoid, has demonstrated therapeutic potential for epilepsy, Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Its anti-inflammatory, antioxidant, and anti-necrotic properties, combined with established safety and tolerability in humans, make it a promising therapeutic agent.”

“Recent research has highlighted CBD’s anti-tumor activity across various cancer types. Studies demonstrate that CBD can inhibit migration, induce apoptosis, and suppress proliferation, invasion, metastasis, and angiogenesis in breast, glioma, lung, and colorectal cancers.”

“Cannabidiol (CBD), an FDA-approved and well-tolerated compound, demonstrates promising antitumor effects by inhibiting cancer growth, metastasis, and angiogenesis, while also alleviating cancer-related symptoms such as pain and nausea.”

https://www.sciencedirect.com/science/article/pii/S0944711325013716?via%3Dihub

Cannabidiol suppresses emergency MDSCs generation by disturbing EEF1B2-mediated C/EBP β protein synthesis in colorectal adenomas

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“Background: Colorectal cancer often develops from adenomas over years, necessitating early intervention. Myeloid-derived suppressor cells (MDSCs) are major immune suppressive cell types in colon cancer development from adenomas through early inflammation-induced emergency myelopoiesis. Cannabidiol (CBD) is reported to function in psychosis, coronavirus infection and some cancers through immune regulation. However, its target and underlying mechanisms in colorectal adenomas are unknown.

Methods: The antitumor effect of CBD was validated in two classical colorectal adenomas models including azoxymethane (AOM)/dextran sulfate sodium salt (DSS) induced mice model and high-fat fed Apcmin/+ mice model. Single-cell RNA sequencing was used to identified the immune environment change after CBD treatment in mice colorectal adenomas. Target responsive accessibility profiling was used to find the target of CBD in MDSCs. Subsequently, multiple immunology assays and molecular biology experiment were employed to explore the adenomas prevention mechanisms of CBD.

Results: Here, we found that CBD prevented the incidence of colorectal adenomas in AOM/DSS model and high-fat diet fed Apcmin/+ mice model. Our single-cell RNA sequencing data and the results of immunofluorescence revealed that CBD treatment significantly decreased the number of MDSCs in both two colon adenomas models. Mechanistically, CBD bound to the guanine nucleotide exchange factor domain of EEF1B2, inhibiting its function in translational elongation and subsequent C/EBPβ synthesis. This disruption suppressed the differentiation and generation of MDSCs, leading to enhanced T-cell activation and prevention of colorectal adenoma progression.

Conclusion: Our findings reveal EEF1B2-mediated C/EBPβ protein synthesis as a crucial pathway in MDSC generation and highlight the potential of CBD as an early intervention strategy for colorectal adenomas.”

https://pubmed.ncbi.nlm.nih.gov/41485775

“In this study, we found that CBD prevented the progression of colorectal adenomas via targeting inhibition the function of EEF1B2 to suppress the generation of MDSC from bone marrow in the condition of adenomas induced systemic inflammation. The underlying mechanism was that EEF1B2 inhibition prevented MDSC differentiation and generation through disturbing the protein synthesis of the key transcription factor C/EBPβ.”

“This study implies that CBD may be a potential compound for clinical translation for colorectal adenomas in clinical use, which makes significant therapeutic implications in the early medical intervention for colorectal adenomas and is an effective strategy to inhibit MDSCs generation and relieve immune suppressive environment in MDSCs involved diseases.”

https://jitc.bmj.com/content/14/1/e013081

Medical Cannabis for Best Supportive Care of Patients Affected by Cancers of the Head and Neck: A Narrative Review

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“Cancers of the head and neck, including malignancies of the oral cavity, pharynx, larynx, and salivary glands, are often associated with severe symptoms that negatively impact quality of life. Patients commonly experience pain, nausea, cachexia (severe weight loss), dysphagia (difficulty swallowing), and xerostomia (dry mouth), all of which can be exacerbated by both the disease and its treatments, such as surgery, radiation, and chemotherapy.

Research has demonstrated that medical cannabis can be effective in managing symptoms such as chronic pain, nausea, vomiting, and anxiety, making it a valuable option in cancer care. Its ability to interact with the endocannabinoid system to reduce nociception (pain perception) and inflammation makes it particularly suitable for the complex symptom burden of patients with head and neck cancer.

This review explores the role of the endocannabinoid system and medical cannabis in mitigating symptoms and improving patient outcomes, as well as its place within the comprehensive care of patients with cancers of the head and neck.”

https://pubmed.ncbi.nlm.nih.gov/41482365

“Medical cannabis is a very interesting and emerging tool in the supportive care of patients with head and neck cancers, offering relief from pain, nausea, loss of appetite, and psychological distress. It complements existing therapies and provides an alternative or adjunct to conventional symptom management strategies, particularly for patients who do not tolerate traditional medications well.”

https://iv.iiarjournals.org/content/40/1/50

Targeting bladder cancer: Potent anti-cancer effects of cannabichromene and delta-9-tetrahydrocannabinol-rich Cannabis sativa strains

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“Objective: This study aimed to explore the anticancer potential of Cannabis sativa (C. sativa) strains, specifically PARIS, Dairy Queen (DQ), and super cannabidiol (sCBD), on bladder cancer cells. Given the increasing interest in cannabinoids like cannabichromene (CBC) and delta-9-tetrahydrocannabinol (THC) for their therapeutic properties, we evaluated their cytotoxic effects on urothelial carcinoma (UC) cell lines and their ability to inhibit cell migration and induce apoptosis in both two-dimensional cell models and three-dimensional ex vivo organ cultures (EVOCs).

Methods: C. sativa strains were screened for their cytotoxicity against UC cell lines (HTB-4 and HTB-9) using XTT assays. Their phytocannabinoid content was analyzed using high-performance liquid chromatography. We employed fluorescence-activated cell-sorting to determine apoptosis and cell cycle, migration assays to determine cell migration, and EVOCs to evaluate the cytotoxic effect on UC. Gene expression was determined by quantitative polymerase chain reaction.

Results: Three commercial C. sativa strains, PARIS, DQ, and sCBD, were found to have the most potent anticancer effects on bladder cancer cells. All extracts contain CBC and THC at different concentrations. In XTT assays on UC cell lines, PARIS had a half-maximal inhibitory concentration (IC50) of 21.58 μg/mL, while DQ and sCBD had similar cytotoxic activity with IC50 values for 48-h treatment of 17.99 μg/mL and 17.88 μg/mL, respectively. DQ and sCBD extracts were found to significantly reduce cell migration and increase the percentage of cells in S phase and G2/M phase within the cell population. In EVOCs, the extracts initiated cell death with the expression of apoptosis-related genes increased following exposure to treatment.

Conclusion: The findings suggest that C. sativa strains PARIS, DQ, and sCBD, containing CBC and THC, exhibit significant anticancer activity against UC cell lines and ex vivo models. These results underscore the therapeutic potential of CBC- and THC-rich C. sativa extracts in bladder cancer treatment.”

https://pubmed.ncbi.nlm.nih.gov/41467200

“This study highlights the potential of commercially available cannabis extracts in inhibiting UC tumors through programmed cell death, the expression of apoptosis-related genes, and cell migration inhibition. The findings emphasize the significance of cannabinoid-specific content over total cannabinoid concentrations in determining their cytotoxic effects. While personalized medicine based on specific strain compositions remains a distant goal, certain cannabinoids like CBC, THC, and CBD show promise in exerting cytotoxic effects.”

“Overall, these findings underscore the potential of cannabis-derived compounds as therapeutic agents in cancer treatment and warrant further investigation.”

https://www.sciencedirect.com/science/article/pii/S2214388225000335?via%3Dihub

Targeting Human Cancer Cells with Cannabidiol (CBD): Apoptotic Cytotoxicity in HeLa, MDA-MB-231, and CaCo-2 Lines

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“Cannabidiol (CBD), a phytocannabinoid derived from Cannabis sativa, has demonstrated therapeutic potential across various diseases, including cancer.

This study evaluates the cytotoxic effects of CBD on three human cancer cell lines (HeLa, MDA-MB-231, and CaCo-2) and two non-cancerous cell lines (HaCaT and HUVEC) used as a control. Cells were treated with CBD at concentrations of 5, 10, and 20 µM for 24, 48, 72, and 96 h. Cytotoxicity was assessed using MTT assays, nuclear morphology was evaluated via DAPI staining, and cell death mechanisms were analyzed through flow cytometry with apoptosis/necrosis markers. The LC50 values at 24 h were determined as follows: HeLa (9.4 µM), MDA-MB-231 (10.3 µM), and CaCo-2 (4.3 µM).

CBD treatment induced morphological changes characteristic of cell stress and death in cancer cells, observed by optical microscopy after 24, 48, 72, and 96 h of exposure. These findings highlight the potential of CBD as an adjunctive therapeutic agent for cancer treatment versus non-malignant cells.”

https://pubmed.ncbi.nlm.nih.gov/41465562

“The findings of this study confirm the potential of CBD as a cytotoxic agent with pro-apoptotic activity in cancer cells.”

“CBD appears to exert a multifaceted mechanism of action on tumor cells, involving both the endocannabinoid system and receptor-independent pathways.”

“In the present study, we demonstrated that CBD induces apoptosis in human cancer cells (HeLa, MDA-MB-231, and CaCo-2) while delaying apoptotic processes in non-malignant control cells (HaCaT and HUVEC). These findings underscore the potential of CBD as an adjunctive therapeutic agent for cancer treatment, highlighting its selective cytotoxic effects on malignant cells with limited impact on non-malignant cells.”

“These results underscore the potential of CBD as an adjunctive therapy in cancer treatment, particularly for colorectal adenocarcinoma, where it exhibited greater efficacy.”

https://www.mdpi.com/1422-0067/26/24/12136


Selective anti-cancer effects of cannabidiol and Δ9-tetrahydrocannabinol via PI3K/AKT/mTOR inhibition and PTEN restoration in ovarian cancer cells

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“Introduction: Ovarian cancer is a highly lethal gynecological malignancy, often diagnosed at advanced stages. Cannabidiol (CBD) and delta-9-tetrahydrocannabinol (THC) demonstrate anti-tumor activity in various cancers including ovarian cancer through multiple signaling pathways and are increasingly explored as adjuncts to chemotherapy. However, the effects of CBD and THC combination treatment and its specific mechanisms remain unclear. This study evaluated the anti-tumor effects of CBD, THC, and their combination on SKOV3 and A2780 ovarian cancer cells, focusing on phosphorylation-dependent regulation of the PI3K/AKT/mTOR pathway.

Methods: SKOV3, A2780, and IOSE cells were treated with CBD, THC, and equimolar CBD: THC combinations. Cytotoxicity was assessed using Sulforhodamine B assay, while synergistic interactions were analyzed by the Chou-Talay method using CompuSyn. Cell cycle distribution and apoptosis were evaluated, and phosphorylation of PI3K, AKT, mTOR, and PTEN was examined by Western blotting.

Results: The CBD: THC combination treatment showed potent, selective cytotoxicity at 48 h, with lower IC50 values than in non-tumor IOSE80 cells. The Chou–Talalay method validated a synergistic effect between CBD and THC. The combination treatment induced cell cycle arrest and enhanced apoptosis. Western blot analysis exhibited that equimolar CBD: THC (2.5:2.5 μM) markedly reduced phosphorylation of PI3K, AKT, and mTOR, while increasing phosphorylation of PTEN, thereby reactivating tumor-suppressive signaling.

Conclusion: These findings highlight that CBD: THC combination treatment effectively inhibited ovarian cancer cell growth and invasion via oncogenic PI3K/AKT/mTOR signaling and reactivates PTEN. The combination may represent a promising targeted therapeutic approach, warranting further in vivo validation to elucidate its clinical potential.”

“Our study elucidated the multi-faceted anti-cancer properties of cannabidiol (CBD) and delta-9-tetrahydrocannabinol (THC), particularly in their combination treatment, by demonstrating potent and selective anti-cancer activities against ovarian cancer cells without harming non-tumor IOSE cells, establishing a favorable therapeutic index.

The combination treatment of CBD and THC exhibited concentration- and ratio-dependent synergy, inhibiting proliferation, and hindering metastatic potential through impaired migration and invasion while inducing apoptosis and attributing to mitochondrial membrane depolarization.

Mechanistically, we revealed that CBD and THC, particularly the CBD: THC combination effectively suppresses the PI3K/AKT/mTOR signaling axis by downregulating the phosphorylation of p-PI3K, p-Akt, and p-mTOR, whereas restoring the function of the tumor suppressor PTEN. This dual modulation of oncogenic and tumor-suppressive pathways endorses the therapeutic potential of CBD: THC treatment as a targeted anti-cancer strategy.

Our findings warrant further in functional phosphatase activity to confirm the reactivation of PTEN lipid phosphatase enzyme, and vivo validation and clinical exploration to optimize cannabinoid-based regimens for ovarian cancer treatment, especially considering the precise concentration- and ration-dependent nature of their interactions.”

https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2025.1693129/full

“Cannabis compounds show unexpected power against ovarian cancer”

“Scientists have discovered that key compounds from cannabis—CBD and THC—show surprisingly strong effects against ovarian cancer cells. Used together, they slow cell growth, reduce colony formation, and may even block the cancer’s ability to spread. Even more promising, the treatment caused minimal harm to healthy cells and appears to work by restoring a disrupted signaling pathway that fuels tumor growth”

https://www.sciencedaily.com/releases/2025/12/251215025315.htm