Cannabichromene Anti-cancer Study

​​Cannabichromene (CBC) Anti-Cancer Research: Key Findings and Mechanisms​​

Cannabichromene (CBC), a non-psychoactive phytocannabinoid derived from Cannabis sativa, has emerged as a promising candidate for cancer therapy. Below is a synthesis of its anti-cancer properties and mechanisms based on recent studies:

Anticancer Mechanisms

​​Induction of Cell Death Pathways​​:

​​Apoptosis​​: CBC activates caspase-3/8/9, triggering programmed cell death in pancreatic, breast, and bladder cancer cells 

​​Ferroptosis​​: Upregulates ferroptosis-related genes (e.g., HMOX1) and depletes glutathione, leading to lipid peroxidation in pancreatic cancer models 

​​Autophagy​​: Modulates LC3-II and Beclin-1 expression, promoting cancer cell self-destruction 

​​Receptor Modulation​​:

​​TRPV1/CB2 Activation​​: CBC binds to TRPV1 (a transient receptor potential channel) and CB2 receptors, enhancing apoptosis and inhibiting tumor growth 

​​ER/AR Downregulation​​: In ER+/AR+ breast cancer, CBC reduces estrogen receptor (ER) and androgen receptor (AR) protein levels, disrupting hormone-driven proliferation .

​​Anti-Inflammatory & Anti-Angiogenic Effects​​:

Suppresses NF-κB and COX-2 pathways, reducing pro-inflammatory cytokines (e.g., TNF-α, IL-6) that promote tumor microenvironment growth 

Inhibits VEGF and matrix metalloproteinases (MMPs), blocking angiogenesis and metastasis 

Efficacy Across Cancer Types

Cancer Type​​	Effects​​	Key Findings​​
Pancreatic Cancer​​	Induces apoptosis and ferroptosis; reduces xenograft tumor growth by 60%	Synergizes with TRPV1/CB2 activation
Breast Cancer (ER+)	Inhibits cell proliferation by 70%; downregulates ER and aromatase	Combines ER/AR targeting with ferroptosis induction
Bladder Cancer​​	Synergizes with THC to cause S-phase arrest and reduce migration by 50%	Inhibits F-actin cytoskeleton integrity, impairing invasion
Skin Cancer​​	Reduces UV-induced inflammation; blocks tumor promotion in mice	Lowers pro-inflammatory cytokines (IL-1α, TNF-α) in sebocytes

Synergistic Effects with Other Cannabinoids

​​CBC + THC​​:

Enhances cytotoxicity in bladder cancer via CB2 receptor activation and apoptosis 

Reduces cell migration and invasiveness in breast cancer models 

​​CBC + CBD​​:

Modulates GPR55 and TRPV1 pathways, amplifying anti-proliferative effects 

Challenges and Future Directions

​​Limitations​​:

Low bioavailability due to rapid metabolism.

Limited clinical data; most studies are preclinical (in vitro/vivo).

​​Research Priorities​​:

​​Clinical Trials​​: Validate efficacy in human trials (e.g., Phase I/II for pancreatic cancer).

​​Formulation Optimization​​: Develop lipid-based carriers to improve stability and delivery.

​​Combination Therapies​​: Explore CBC with chemotherapy (e.g., gemcitabine) or immunotherapy.

Notable Studies

​​Pancreatic Cancer (2025)​​: CBC upregulates ferroptosis genes (HMOX1, ACSL4) and induces caspase-mediated apoptosis in MiaPaCa-2 cells 

​​Breast Cancer (2025)​​: CBC downregulates ERα and AR protein levels by 80%, suppressing luminal A subtype growth .

​​Bladder Cancer (2021)​​: CBC + THC reduces T24 cell viability by 65% via S-phase arrest and F-actin disorganization 

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Conclusion

Cannabichromene (CBC) exhibits multifaceted anti-cancer activity through apoptosis induction, receptor modulation, and anti-inflammatory effects. While preclinical data are robust, clinical translation requires further exploration of its pharmacokinetics and synergistic potential. Future studies should prioritize patient stratification (e.g., ER+/HER2- breast cancer) and novel delivery systems to maximize therapeutic benefits.

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