Research

Cannabinoids protect against sunburn and skin cancer because of the CB1 receptors in our skin.

THC to cure skin cancer?
Well, not just skin cancer. It has been documented that THC from the cannabis plant attacks cancerous and mutated cells while leaving healthy cells unharmed.

Anti-Cancer Properties of THC – Research in Print:
[1] Parolaro and Massi. 2008. Cannabinoids as a potential new drug therapy for the treatment of gliomas. Expert Reviews of Neurotherapeutics 8: 37-49
[2] Guzman et al. 2006. A pilot clinical study of delta-9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. British Journal of Cancer.
[3] Galanti et al. 2007. Delta9-Tetrahydrocannabinol inhibits cell cycle progression in human glioblastoma multiforme cells. Acta Oncologica 12: 1-9.
[4] Calatozzolo et al. 2007. Expression of cannabinoid receptors and neurotrophins in human gliomas. Neurological Sciences 28: 304-310.
[5] Cannabinoids selectively inhibit proliferation and induce death of cultured human glioblastoma multiforme cells. Journal of Neurooncology. 2005
http://www.ncbi.nlm.nih.gov/pubmed/16078104?dopt=Citation
[6] Cannabinoids and cancer. Mini-Reviews in Medicinal Chemistry. 2005
http://www.ingentaconnect.com/content/ben/mrmc/2005/00000005/00000010/art00006
[7] The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells. Gut. 2005 http://gut.bmj.com/cgi/content/abstract/54/12/1741
[8] Cannabinoid receptor as a novel target for the treatment of prostate cancer. Cancer Research. 2005 http://cancerres.aacrjournals.org/cgi/content/abstract/65/5/1635
[9] Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines. Journal of Pharmacology And Experimental Therapeutics. 2004
http://jpet.aspetjournals.org/cgi/content/abstract/jpet.103.061002v1
[10] Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Cancer Research. 2004 http://cancerres.aacrjournals.org/cgi/content/full/64/16/5617
[11] Delta-9 tetrahydrocannabinol (THC) inhibits lytic replication of gamma oncogenic herpesviruses in vitro. BMJ Medicine. 2004
http://www.biomedcentral.com/1741-7015/2/34/abstract
[12] Cannabinoids: potential anticancer agents. Nature Reviews Cancer. 2003
http://americanmarijuana.org/Guzman-Cancer.pdf
[13] Inhibition of tumor angiogenesis by cannabinoids. The FASEB Journal. 2003
http://www.fasebj.org/cgi/content/full/17/3/529
[14] Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. Journal of Clinical Investigation. 2003
http://www.jci.org/articles/view/16116/version/1
[15] Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation. Nature Medicine. 2000
http://www.annieappleseedproject.org/anacofcanrat.html
[16] Delta9-tetrahydrocannabinol induces apoptosis in C6 glioma cells. FEBS Letters. 1998 http://www.febsletters.org/article/PIIS0014579398010850/abstract
[17] The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation. Proceedings of the National Academy of Sciences of the USA. 1998
[18] Toxicology and Carcinogenesis Studies of 1 trans-delta-9-tetrahydrocannabinol in F344N/N Rats and BC63F1 Mice. National Institutes of Health National Toxicology Program, NIH Publication No. 97-3362. 1996.
[19] Antineoplastic activity of cannabinoids. Journal of the National Cancer Institute. 1975 http://www.ukcia.org/research/AntineoplasticActivityOfCannabinoids/default.html

Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1.

Cannabinoids inhibit cancer cell invasion via increasing tissue inhibitor of matrix metalloproteinases-1 (TIMP-1). This study investigates the role of intercellular adhesion molecule-1 (ICAM-1) within this action. In the lung cancer cell lines A549, H358, and H460, cannabidiol (CBD; 0.001-3 μM) elicited concentration-dependent ICAM-1 up-regulation compared to vehicle via cannabinoid receptors, transient receptor potential vanilloid 1, and p42/44 mitogen-activated protein kinase. Up-regulation of ICAM-1 mRNA by CBD in A549 was 4-fold at 3 μM, with significant effects already evident at 0.01 μM. ICAM-1 induction became significant after 2 h, whereas significant TIMP-1 mRNA increases were observed only after 48 h. Inhibition of ICAM-1 by antibody or siRNA approaches reversed the anti-invasive and TIMP-1-upregulating action of CBD and the likewise ICAM-1-inducing cannabinoids Δ(9)-tetrahydrocannabinol and R(+)-methanandamide when compared to isotype or nonsilencing siRNA controls. ICAM-1-dependent anti-invasive cannabinoid effects were confirmed in primary tumor cells from a lung cancer patient. In athymic nude mice, CBD elicited a 2.6- and 3.0-fold increase of ICAM-1 and TIMP-1 protein in A549 xenografts, as compared to vehicle-treated animals, and an antimetastatic effect that was fully reversed by a neutralizing antibody against ICAM-1 [% metastatic lung nodules vs. isotype control (100%): 47.7% for CBD + isotype antibody and 106.6% for CBD + ICAM-1 antibody]. Overall, our data indicate that cannabinoids induce ICAM-1, thereby conferring TIMP-1 induction and subsequent decreased cancer cell invasiveness.

Bublitz K., Ramer R. Read Full Text Here 2012 Apr;26(4):1535-48. doi: 10.1096/fj.11-198184. Epub 2011 Dec 23.

 

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