Cannabinoids and Cancer Cells
Cannabinoids have been shown to stop the spread of cancer cells in vitro.
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Cancer is a type of inflammatory disease where immune cells infiltrate into the tumor site and secrete factors which enhance the prospects of proliferation, angiogenesis and metastasis.
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The anti-inflammatory ability of cannabinoids is twice that of cortisone.
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When cancer cells form in certain areas of the body, cannabinoid receptor sites (CB1 and CB2) form and multiply in the cancer cells and surrounding tissues.
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Cannabinoids have been proved to be anti-proliferative and apoptotic drugs.
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Apoptosis: In multicellular organisms, cells that are no longer needed or are a threat to the organism are destroyed by a tightly regulated cell suicide process known as programmed cell death.
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Cannabinoids inhibit tumor growth in animal models by inducing apoptosis of tumor cells and impairing tumor angiogenesis.
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These results have been demonstrated in vitro to occur in lung, brain, breast and prostate tissue affected by cancer.
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Cannabinoids derived from different sources regulate different signaling pathways, and modulate different tumor cell types.
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It is important to understand which of the cannabinoid receptors are expressed and activated in different tumors as each receptor follows a different signaling mechanism.
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The administration of single cannabinoids might produce limited relief compared to the administration of crude extract of plant containing multiple cannabinoids, terpenes, and flavonoids.
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This finding supports the "entourage" hypothesis that states that multiple cannabinoids working together are more effective than isolated cannabinoids.
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Current FDA drugs are mostly focused on isolating singular compounds and synthesizing said compounds. This isolation of individual compounds does not seem to be effective in the way that multiple cannabinoids working in concert are.
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Breast Cancer and Cannabinoids:
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Cannabinoids modulate the growth of hormone sensitive breast cancer cells
Cannabinoids and Prostate Cancer:
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CB1 and CB2 expression levels were higher in prostate cancer tissues and several cell lines
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This increased expression of receptors is a way for the body to provide an "expanded landing" surface for cannabinoids to activate said receptors to facilitate apoptosis of cancer cells.
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THC, cannabidiol (CBD), anandamide, 2-AG, and its stable analogue noladin have exerted anti-proliferative, apoptotic and anti-invasive effects in different prostate cancer cells both in vitro and in vivo.
Cannabinoids and Lung Cancer:
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Blocking FAAH increases the levels of AEA, which in turn inhibits EGFR signaling pathway, ultimately leading to cell cycle arrest and apoptosis.
Cannabinoids and Skin Cancer:
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CB1 and CB2 receptors are expressed in normal skin and skin tumors of mice and humans
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Activation of CB1/CB2 receptors induced the apoptotic death of tumorigenic epidermal cells without affecting the nontransformed epidermal cells.
Cannabinoids and Pancreatic Cancer:
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CB1 and CB2 receptors were expressed in normal and pancreatic cancer tissues.
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Cannabinoid administration leads to apoptosis of pancreatic tumor cells via CB2 receptors and ceramide-dependent up-regulation of p8 and ATF-4 and TRB3 stress–related genes.
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Another study showed that CB1 receptor antagonist AM251–induced cell death in pancreatic MIAPaCa-2 cells occurred via receptor-independent manner.
Cannabinoids and Bone Cancer:
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Breast cancer and prostate cancer mainly metastasize to bone which act as a fertile soil for the growth of secondary tumors.
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The skeletal endocannabinoid system plays a significant role in regulating bone mass and bone turnover.
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Synthetic cannabinoid WIN 55,212-2 was demonstrated to attenuate tumour-evoked mechanical hyperalgesia following local (intraplantar) administration through activation of CB1 and CB2 receptors.
Cannabinoids and Glioma
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In glioblastoma endothelial cells, CB1 and CB2 receptors were present in about 38% and 54% of the cells respectively.
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CB2 expression levels were higher in glioblastoma tissue in comparison to CB1. Selective CB2 agonists may become important targets for the treatment of glioma.
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Cannabinoids inhibit tumor growth in animal models by inducing apoptosis of tumor cells and impairing tumor angiogenesis.
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Administration of Δ9-THC and synthetic cannabinoid JWH-133 inhibits MMP-2 expression in in vivo model of glioma.
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CBD treatment induces apoptosis in glioma cells in vitro and tumor regression in vivo through activation of caspases and reactive oxygen species via receptor-independent manner.
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Studies reveal that CBD induced TRPV2-dependent Ca2+ influx, which triggers the drug uptake and synergizes with cytotoxic agents to induce apoptosis of glioma cells.
Cannabinoids and Lymphoma:​
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Cannabinoid receptor ligands mediate growth inhibition and cell death in mantle cell lymphoma
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Δ9-THC inhibits cell viability and increased apoptosis both in vitro in EL4 and MCL cells and EL4 tumor-bearing mice.
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Paraptosis-like cell death, a third type of a programmed cell death, occurred in response to cannabinoids.
Cannabinoids and Oral Cancer:
Cannabinoids and Head and Neck Cancer:
Cannabinoids and Thyroid Carcinoma: