In one study, it was shown that pancreatic cancer cells (MiaPaCa2, Panc1, Capan2, and BxPc3 cell lines) can effectively be killed by THC (2 μM and higher concentrations) (Carracedo et al., 2006).
Furthermore, the authors found that both cannabinoid receptors CB1 and CB2 are expressed by the pancreatic tumor biopsies and cell lines. In mice, the growth of pancreatic tumor cells can be decreased by THC (15 mg/kg/d). Also, THC was seen to induce apoptosis of pancreatic cells (Carracedo et al., 2006).
In human pancreatic cancer cells (MIA PaCa-2), it was shown that cell death can be triggered by various agonists and antagonists via a receptor-independent mechanism (Fogli et al., 2006).
In human patients, decreased survival was connected to high expression of CB1 in pancreatic cancer cells. Similarly, decreased survival was connected to low levels of endocannabinoid-degrading enzyme FAAH and MAGL. Furthermore, levels of Anandamide and 2AG were found to be unaffected in pancreatic cancer. Finally, increased survival and strong pain symptoms were found to be connected to low CB1 receptor levels in nerves (Michalski et al., 2008). More research is needed to elucidate the mechanistic value of these correlations.
AMP-kinase and ROS-dependent autophagy of cancer cells can be triggered by cannabinoids specific for the CB1 (ACPA) and CB2 (GW) receptors in Panc1 cells (Dando et al., 2013).
Combination of CB1 and CB2 agonists with the anti-cancer drug Gemcitabine synergistically suppressed pancreatic adenocarcinoma cell proliferation and enhanced intracellular ROS production (Donadelli et al., 2011).