Prostate cancer cells highly express CB1 and CB2 receptors.
High expression of these receptors was shown to increase in the most aggressive cancer cells (Orellana-Serradell et al., 2015; Thors et al., 2010).
Expression of receptors such as CB1, CB2, and TRPV1 may be used as a prognostic factor in prostate cancer cells (Chung et al., 2009; Czifra et al., 2008; Fowler et al., 2010, 2013).
It was shown that prostate cancer cells can be suppressed by cannabinoids such as 2-AG, Anandamide, THC, and CBD via CB1 receptor inducing phosphatase-dependent apoptosis (De Petrocellis et al., 2013; Mimeault et al., 2003; Nithipatikom et al., 2004, 2011; Sreevalsan et al., 2011).
In vivo and in vitro models of prostatic cancer cells, CB1 and CB2 agonists also exhibit anti-proliferative activities (De Petrocellis et al., 2013; Mimeault et al., 2003; Nithipatikom et al., 2011; Olea-Herrero et al., 2009a, 2009b).
It has also been reported that cell proliferation can be regulated by the novel receptor GPR55 (Piñeiro et al., 2011).
Cannabinoid receptor-induced apoptosis and anti-proliferative effects can be regulated by Erk and Akt signaling pathways (Cipriano et al., 2013; Orellana-Serradell et al., 2015; Sarfaraz et al., 2006).
Furthermore, it was demonstrated that synthetic cannabinoids exhibit apoptosis and anti-proliferation activity through oxidative stress, PPARy, and CB1 receptors (Morales et al., 2013; Sarfaraz et al., 2005).