The effect of CBD(BDS) botanical cannabinoid extraction on MCF-7 human breast carcinoma cells.

The use of cannabinoids in cancer treatment has recently attracted attention (Alexander et
al., 2009). A number of studies have shown that the apoptosis or reduced growth induced
in tumour cells by cannabinoids involves an increase in the expression of CB2 receptors
(Alexander et al., 2009; Pisanti et al., 2009). The aim of the present study was to
investigate the potential anti-tumour activity of CBD (BDS), a botanical cannabinoid
extract on breast tumour cells. MCF-7 cells (American Type Culture Collection) were
grown and maintained in RPMI 1640 medium supplemented with 10% fetal bovine
serum at 37oC, 5% CO2 .The cells were plated in 96-well culture plates at a density of
1x104 cells/well and allowed to adhere at 37oC for 24 hours. The following day, various
doses of extract in the absence and presence of AM251, SR144528 and capsazepine,
were added to the cells and further incubated for 4 days. Then the supernatant was
removed and MTT (3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) was
added for 4 hours. The ability of cells to form formazan crystals by active mitochondrial
respiration was determined by using a Microplate reader after dissolving the crystals in
DMSO. Cytotoxicity was expressed as a relative percentage of the absorbance measured
at 540 nm in the control and extract-treated cells.
CBD (BDS) extract induced dose-dependent cytotoxic effects on MCF-7 cells with an
IC50 of 0.046 mg/ml. Pre-treatment with AM251, SR144528 and Capsazepine, CB1,
CB2 and TRPV1 receptor antagonists, respectively, did not reverse the cytotoxicity
afforded by CBD (BDS). Single application of antagonists alone or vehicle did not affect
the survival rate of the MCF7 cells. The data suggest the unlikely involvement of CB1,
CB2 and TRPV1 receptors in mediating CBD (BDS)-induced apoptosis in MCF-7
tumour cells. Further experiments are required to investigate the receptor type/subtypes
involvement and the mechanism of cell death.