Cannabigerol Treatment Shows Antiproliferative Activity and Causes Apoptosis of Human Colorectal Cancer Cells
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Objectives: To determine growth inhibitory and anti-cancer effects of Cannabigerol (CBG) in human colorectal cancer cells. Methods: Anti-proliferative effect of CBG was examined using MTT assay and two colorectal cancer cells (SW480 and LoVo cells). Cell death ratio was analyzed using Annexin V/ PI staining experiment. Cell cycle distribution was analyzed using flow cytometry. We also performed western blot analysis on apoptotic marker proteins. Results: CBG showed growth inhibitory effect in colorectal cancer cells using MTT assay. IC50 concentration of CBG was 34.89 μM in SW480 cells and 23.51 μM in LoVo cells. Annexin V/PI staining showed that CBG treatment increased apoptotic cells from 4.8% to 31.7% in SW480 cells and from 7.7% to 33.9% in LoVo cells. Flow cytometry confirmed that CBG increased sub G1 population via G1 arrest in both SW480 and LoVo cells. Western blot analysis showed that CBG increased expression levels of cell death-related proteins such as cleaved PARP-1, cleaved caspase 9, p53, and caspase 3. Conclusion: CBG treatment shows antiproliferative activity and causes apoptosis of colorectal cancer cells, suggesting that CBG is applicable as a promising anticancer drug.
Abstract
Objectives: To determine growth inhibitory and anti-cancer effects of Cannabigerol (CBG) in human colorectal cancer cells. Methods: Anti-proliferative effect of CBG was examined using MTT assay and two colorectal cancer cells (SW480 and LoVo cells). Cell death ratio was analyzed using Annexin V/ PI staining experiment. Cell cycle distribution was analyzed using flow cytometry. We also performed western blot analysis on apoptotic marker proteins. Results: CBG showed growth inhibitory effect in colorectal cancer cells using MTT assay. IC50 concentration of CBG was 34.89 μM in SW480 cells and 23.51 μM in LoVo cells. Annexin V/PI staining showed that CBG treatment increased apoptotic cells from 4.8% to 31.7% in SW480 cells and from 7.7% to 33.9% in LoVo cells. Flow cytometry confirmed that CBG increased sub G1 population via G1 arrest in both SW480 and LoVo cells. Western blot analysis showed that CBG increased expression levels of cell death-related proteins such as cleaved PARP-1, cleaved caspase 9, p53, and caspase 3. Conclusion: CBG treatment shows antiproliferative activity and causes apoptosis of colorectal cancer cells, suggesting that CBG is applicable as a promising anticancer drug.
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