Cannabis sativa L. and Nonpsychoactive Cannabinoids: Their Chemistry and Role against Oxidative Stress, Inflammation, and Cancer

Figure 3

General representation of the signaling pathways involved in CBD anticancer mediated effects. Cannabinoid-induced apoptosis relies on the stimulation of endoplasmic reticular (ER) stress and through stimulation of TRPV channel. The signaling route involving the arrest of cell proliferation is mediated by the antagonism mainly on GPR55, which causes an inhibition of the activation of ERK pathway; in addition, the block of ROCK activation might be responsible for the antimigratory effect elicited by cannabidiol. CBD, cannabidiol; CB₂, cannabinoid receptor 2; TRPV1/2, receptor potential channel subfamily V members 1 and 2; GPR55, orphan G-protein coupled receptor 55; ROS, reactive oxygen species; ER, endoplasmic reticulum; p8, protein p8 (Nuclear Protein 1, NUPR1); CHOP, CCAAT/-enhancer-binding protein homologous protein; ATF2, activating transcription factor 2; CREB, cAMP response element-binding protein; Akt, protein kinase B; ROCK Rho-associated protein kinase; NFAT, nuclear factor of activated T-cells; NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells; PKC, protein kinase C; P38, mitogen-activated protein kinases.