cannabinoids as THC and CBD have shown anti cancer properties in several studies through CB1 and CB2 receptors (Caffarel et al., 2008; Massi et al., 2013).
CBD can inhibit cancer cell growth and proliferation through autophagy process without affecting non-cancer cells (Elbaz et al., 2015; Shrivastava et al., 2011).
This anti cancer properties are related to CBD-induced ID1 protein inhibition (Murase et al., 2014). Also, CBD can improve chemotherapy efficacy like in the case of the anti cancer drug Paclitaxel, which is combined with CBD to treat the associated neuropathic pain to the drug through 5HT1A receptor(Ward et al., 2014).
Caffarel, M.M., Moreno-Bueno, G., Cerutti, C., Palacios, J., Guzman, M., Mechta-Grigoriou, F., and Sanchez, C. (2008). JunD is involved in the antiproliferative effect of Delta9-tetrahydrocannabinol on human breast cancer cells. Oncogene 27, 5033–5044.
Elbaz, M., Nasser, M.W., Ravi, J., Wani, N.A., Ahirwar, D.K., Zhao, H., Oghumu, S., Satoskar, A.R., Shilo, K., Carson, W.E., et al. (2015). Modulation of the tumor microenvironment and inhibition of EGF/EGFR pathway: novel anti-tumor mechanisms of Cannabidiol in breast cancer. Mol. Oncol. 9, 906–919.
Massi, P., Solinas, M., Cinquina, V., and Parolaro, D. (2013). Cannabidiol as potential anticancer drug. Br. J. Clin. Pharmacol. 75, 303–312.
Murase, R., Kawamura, R., Singer, E., Pakdel, A., Sarma, P., Judkins, J., Elwakeel, E., Dayal, S., Martinez-Martinez, E., Amere, M., et al. (2014). Targeting multiple cannabinoid anti-tumour pathways with a resorcinol derivative leads to inhibition of advanced stages of breast cancer. Br. J. Pharmacol. 171, 4464–4477.
Shrivastava, A., Kuzontkoski, P.M., Groopman, J.E., and Prasad, A. (2011). Cannabidiol Induces Programmed Cell Death in breast cancer Cells by Coordinating the Cross-talk between Apoptosis and Autophagy. Mol. cancer Ther. 10, 1161–1172.
Ward, S.J., McAllister, S.D., Kawamura, R., Murase, R., Neelakantan, H., and Walker, E.A. (2014). Cannabidiol inhibits paclitaxel-induced neuropathic pain through 5-HT(1A) receptors without diminishing nervous system function or chemotherapy efficacy. Br. J. Pharmacol. 171, 636–645.