**Cannabidiol (CBD) Exhibits Dose-Dependent Anti-Cancer Effects Across Multiple Cancer Types**
Research demonstrates that cannabidiol (CBD) consistently produces dose-dependent reductions in cancer cell viability, proliferation, migration, invasion, and tumor growth while inducing apoptosis and cell cycle arrest in various preclinical models. Below is a compilation of key studies highlighting these effects across different cancers, with specific dose ranges and outcomes.
### Breast Cancer
**CBD Induces Concentration-Dependent Apoptosis and Reduces Viability in Breast Cancer Cell Lines**
CBD treatment (0–10 μM for 24 hours) significantly decreased cell viability in both estrogen receptor-positive (e.g., MCF-7, T-47D) and triple-negative (e.g., MDA-MB-231) breast cancer lines in a concentration-dependent manner. It triggered apoptosis (measured by Annexin V staining) and inhibited survival pathways independently of CB1/CB2 receptors at lower doses, with partial CB2 involvement at higher concentrations. Higher doses enhanced pro-apoptotic proteins like p53, Caspase-3, and Bax.
**CBD and THC Mixture Shows Dose- and Time-Dependent Anti-Proliferative and Pro-Apoptotic Effects in Breast Cancer**
In MDA-MB-231 and MCF-7 cells, CBD/THC (3:1 ratio, 12.5–17.5 μg/mL) inhibited proliferation dose- and time-dependently over 24–48 hours, reducing viability by up to 86% at higher doses. It increased apoptotic cells (Annexin V/PI staining) and altered cell cycle progression, with stronger effects in triple-negative lines.
### Colorectal Cancer
**CBD Represses Viability and Induces G1 Arrest and Apoptosis in Colorectal Cancer Cells**
CBD (0–40 μM for 24–48 hours) reduced viability in multiple human colorectal cancer lines (e.g., HCT116, SW480) in a dose-dependent manner, with IC50 values ranging from 4.7–20 μM. It caused G1-phase cell cycle arrest, elevated apoptosis markers, and endoplasmic reticulum stress.
**CBD Reduces Viability and Enhances Apoptosis in p53-Dependent Colorectal Cancer Models**
In HCT116 (p53 wild-type and knockout) and other lines, CBD (5–20 μM for 24–48 hours) lowered viability dose-dependently (IC50 7.9–24.3 μM). Sensitivity was higher in p53 wild-type cells, with increased ROS, mitochondrial disruption, and caspase activation at higher doses.
### Glioma/Glioblastoma
**CBD Is Cytotoxic and Perturbs Mitochondrial Function in Glioma Cells**
CBD (0–20 μg/mL for 96 hours) inhibited proliferation and induced cytotoxicity in human (U87MG, U373MG) and canine glioma lines in a dose-dependent manner (IC50 4.9–8.2 μg/mL). It reduced oxygen consumption and ATP production dose-dependently within 2 hours, leading to swollen mitochondria and apoptosis (rescued by apoptosis inhibitors).
**CBD Suppresses Glioma Cell Viability in Combination Contexts**
CBD and BCNU each produced dose-dependent suppression of T98G glioma cell viability, with CBD enhancing overall anti-tumor activity through apoptotic pathways.
### Prostate Cancer
**CBD Decreases Viability and Induces Apoptotic Cell Death in Prostate Cancer Cells**
In PC3 cells, CBD (0.03–10 μM for 48 hours) reduced viability dose-dependently (up to 37% at higher doses) and activated caspase-3/7 pathways, increasing DNA fragmentation, ROS, and pro-apoptotic Bax while altering mitochondrial potential.
### Lung Cancer and Other Solid Tumors
**CBD Inhibits Long-Term Survival in Multiple Cancer Cell Lines Including Lung Carcinoma**
CBD showed dose-dependent killing in large cell lung carcinoma (H460, IC50 8.47 μM), metastatic breast (MDA-MB-231, IC50 8.35 μM), melanoma (A375, IC50 2.45 μM), cervical carcinoma, and osteosarcoma lines after 7–10 days. Apoptosis was confirmed via PARP cleavage, with ER stress as a key mechanism.
**CBD Reduces Proliferation, Migration, and Invasion in Head and Neck Squamous Cell Carcinoma**
CBD treatment decreased HNSCC cell viability, migration, and invasion dose- and t