The use of cannabinoids as anticancer agents – ScienceDirect

Administration of THC and other cannabinoids exert anticancer actions in animal models of cancer.

nHighlight:THC and other cannabinoid receptor-ligands induce cancer cell death and inhibit tumor angiogenesisnHighlight:Cannabinoids enhance the anticancer activity of other antineoplastic agentsnHighlight:Δ9-tetrahydrocannabinol (THC), the main active component of Cannabis sativa exerts its effects by mimicking endogenous substances – the endocannabinoids anandamide (Devane et al., 1992) and 2-arachidonoylglycerol (2-AG) nHighlight:CB1 and CB2nHighlight:TRPV1nHighlight:orphan G protein-coupled receptor GPR55nHighlight:peroxisome proliferator-activated receptors (PPARs)nHighlight:cannabinoids effects in the central nervous system rely on CB1 receptor activationnHighlight:CB2 receptor was initially described to be present in the immune systemnHighlight:cannabinoids have been shown to alleviate nausea and vomit induced by chemotherapynHighlight:Cannabinoids also inhibit painnHighlight:appetite stimulation and attenuation of wasting nHighlight:In many cases, these reports show that levels of endocannabinoids and their receptors are increased in cancer, a situation that frequently correlates with tumor aggressivenessnHighlight:anandamide and 2-AG have been shown to be over-expressed in several types of tumorsnHighlight:circulating endocannabinoid levels have been associated with increased disease progressionnHighlight:CB1 receptor was found to be upregulated in Hodgkin lymphoma cellsnHighlight:CB1 receptor levels are also increased and correlate with disease severity in human epithelial ovarian tumorsnHighlight:CB2 receptor, a correlation between its expression, histologic grade and prognosis has been demonstrated in breast cancer (Caffarel et al., 2006) and gliomanHighlight:Higher histological grades of human glioblastomas, breast, pancreatic and skin cancers have been reported in association with increased GPR55 expressionnHighlight:silencing of GPR55 reduced the proliferation of tumornHighlight:cannabinoids (endogenous, phytocannabinoids or synthetic) act as efficient anti-tumoral agents in a wide range of cancer cells.nHighlight:cannabinoid receptor agonists (derived from the plant, like THC, endogenous like 2-AG and anandamide or synthetic — with similar or different affinity for CB1 and CB2 receptors like WIN 55,2121-2 or JWH-133) exert antitumor effectsnHighlight:Cannabinoid treatment promotes cancer cell death, impair tumor angiogenesis and block invasion and metastasisnHighlight:autophagy-mediated apoptotic cancer cell deathnHighlight:Autophagy is considered primarily a cytoprotective mechanism, although its activation can also lead to cell deathnHighlight:Unlike the cell death-promoting action of cannabinoids on cancer cells, the viability of normal (non-transformed) cells is unaffected or – under certain conditions – even enhanced by cannabinoid challengenHighlight:stimulation of cannabinoid receptors seems to be coupled to the activation of different signaling mechanisms in transformed and non-transformed cells.nHighlight:Cannabidiol [CBD; a plant-derived cannabinoid with low affinity for cannabinoid receptorsnHighlight:trigger apoptosis in cancer cellsnHighlight:CBD produces these anticancer actions – at least in part – via enhanced production of reactive oxygen speciesnHighlight:CBD may activate TRPV2 receptors to promote cancer cell deathnHighlight:cannabinoids to inhibit the stimulation of the vascular endothelial growth factor (VEGF) pathway.nHighlight:VEGFR1 and VEGFR2), have been shown to be down-regulated in response to treatment with cannabinoids in different cancer typesnHighlight:cannabinoid receptor activation inhibits migration and proliferation, and induces apoptosis in vascular endothelial cellsnHighlight:reduce the formation of distant tumor masses nHighlight:inhibit migration, adhesion and invasivenessnHighlight:autophagy-mediated cancer cell deathnHighlight:CBD exerts a significant anticancer effect – and specifically the inhibition of invasiveness and mestastasisnSticky notes:“Significant’nHighlight:CBD relies – at least partially – on the downregulation of ID-1nHighlight:Combination of THC with pharmacological inhibitors of ALK (or genetic inhibition of MDK) enhances cannabinoid action in resistant tumorsnHighlight:targeting EGFR pathway may also be a therapeutic strategy to enhance cannabinoid anticancer activitynHighlight:gemcitabine (the benchmark agent for the treatment of pancreatic cancer) acted synergistically with different cannabinoid agonists to reduce cell viabilitynHighlight:C. sativa produces ~ 108 different cannabinoidsnHighlight:stimulation of autophagy and apoptosisnHighlight:inhibition of cell proliferation nHighlight:decreased VEGF signalingnHighlight:MMP-2 down-regulation n]]>

Picture of About Dr. Nathan Goodyear
About Dr. Nathan Goodyear

Dr. Nathan Goodyear, a medical doctor with years of experience in the field of integrative cancer care, has announced the launch of an online training program. This program, available on his new website, will provide individuals with access to video trainings led by Dr. Goodyear himself, covering a range of topics related to integrative cancer care. These trainings will include information on the latest research and techniques in the field, as well as guidance on how to incorporate these approaches into a patient’s overall cancer treatment plan. With this online program, Dr. Goodyear hopes to make his expertise and knowledge more widely accessible, and help more people understand the benefits of integrative cancer care.


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