12.5.6 Signaling Pathways Associated With Cannabinoid Receptor
Activation (Fig. 12.3)
12.5.7 Clinical Trials
Preclinical models proposed the anticancer role of cannabinoids, notably by
inhibiting cell proliferation, angiogenesis, metastasis, and invasiveness. Several
cell signaling pathways that are involved in the antitumor activity of cannabinoids
implicated the connection between ESC system and cancer. There are eight ongoing/
completed clinical trials representing the antitumor effect of cannabinoids in various
cancer types. Apart from their antitumor activities, these trials also aimed to assess
Fig. 12.3 Schematic representation of cannabinoid receptor-mediated downstream signaling cas-
cade in various cancers: (i) non-cannabinoid receptors after interaction with cannabinoid ligands
activate the JAK/STAT pathway. (ii) Apoptosis is induced by activation of CB1 receptor and
increase in the ratio of Bax/bcl-2 occurs, which in response upregulates the expression of PARP and
caspases 3 and 9. (iii) CB1 receptors act through Gi/o protein and activate ERK1/2 which in
response activate p27/kip1 protein and bring induced cell cycle arrest via inactivation of cyclins.
(iv) CB1 and CB2 receptors interact with Gi/o protein which inhibits adenylyl cyclase and
subsequently
elicits
the
cAMP
accumulation,
which
ultimately
leads
to
apoptosis.
(v) Downregulation of MMP-2, MMP-7, MMP-9, and VEGF-A leads to inhibition of angiogenesis,
metastasis, and invasion of cells. (vi) CB2 receptors stimulate the release of ceramide (second
messenger) which inhibits AKT signaling following mTOR pathway causing programmed cell
death. (vii) Additionally, proapoptotic protein TRB3 is activated which in response induces ER
stress in a cell and ultimately causes apoptosis. (viii) CB2 receptor also leads to inhibition of
FAK-src pathway which eventually induces apoptosis. (ix) Apart from cannabinoid receptors,
non-CB receptors are involved in cell lysis via activation of lymphokine-activated killer
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