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The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids.

Abstract

As a therapeutic agent, most people are familiar with the palliative effects of the primary psychoactive constituent of Cannabis sativa (CS), Δ(9)-tetrahydrocannabinol (THC), a molecule active at both the cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptor subtypes. Through the activation primarily of CB1 receptors in the central nervous system, THC can reduce nausea, emesis and pain in cancer patients undergoing chemotherapy. During the last decade, however, several studies have now shown that CB1 and CB2 receptor agonists can act as direct antitumor agents in a variety of aggressive cancers. In addition to THC, there are many other cannabinoids found in CS, and a majority produces little to no psychoactivity due to the inability to activate cannabinoid receptors. For example, the second most abundant cannabinoid in CS is the non-psychoactive cannabidiol (CBD). Using animal models, CBD has been shown to inhibit the progression of many types of cancer including glioblastoma (GBM), breast, lung, prostate and colon cancer. This review will center on mechanisms by which CBD, and other plant-derived cannabinoids inefficient at activating cannabinoid receptors, inhibit tumor cell viability, invasion, metastasis, angiogenesis, and the stem-like potential of cancer cells. We will also discuss the ability of non-psychoactive cannabinoids to induce autophagy and apoptotic-mediated cancer cell death, and enhance the activity of first-line agents commonly used in cancer treatment.

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  • Authors+Show Affiliations

    ,

    California Pacific Medical Center Research Institute, 475 Brannan Street, Suite 220, San Francisco, CA, 94107, USA, mcallis@cpmcri.org.

    ,

    Source

    MeSH

    Animals
    Antineoplastic Agents, Phytogenic
    Cannabinoids
    Humans
    Neoplasms
    Plant Extracts
    Receptor, Cannabinoid, CB1
    Receptor, Cannabinoid, CB2

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    25916739

    Citation

    McAllister, Sean D., et al. "The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids." Journal of Neuroimmune Pharmacology : the Official Journal of the Society On NeuroImmune Pharmacology, vol. 10, no. 2, 2015, pp. 255-67.
    McAllister SD, Soroceanu L, Desprez PY. The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids. J Neuroimmune Pharmacol. 2015;10(2):255-67.
    McAllister, S. D., Soroceanu, L., & Desprez, P. Y. (2015). The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids. Journal of Neuroimmune Pharmacology : the Official Journal of the Society On NeuroImmune Pharmacology, 10(2), pp. 255-67. doi:10.1007/s11481-015-9608-y.
    McAllister SD, Soroceanu L, Desprez PY. The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids. J Neuroimmune Pharmacol. 2015;10(2):255-67. PubMed PMID: 25916739.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids. AU - McAllister,Sean D, AU - Soroceanu,Liliana, AU - Desprez,Pierre-Yves, Y1 - 2015/04/28/ PY - 2014/12/16/received PY - 2015/03/30/accepted PY - 2015/4/29/entrez PY - 2015/4/29/pubmed PY - 2016/4/2/medline SP - 255 EP - 67 JF - Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology JO - J Neuroimmune Pharmacol VL - 10 IS - 2 N2 - As a therapeutic agent, most people are familiar with the palliative effects of the primary psychoactive constituent of Cannabis sativa (CS), Δ(9)-tetrahydrocannabinol (THC), a molecule active at both the cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptor subtypes. Through the activation primarily of CB1 receptors in the central nervous system, THC can reduce nausea, emesis and pain in cancer patients undergoing chemotherapy. During the last decade, however, several studies have now shown that CB1 and CB2 receptor agonists can act as direct antitumor agents in a variety of aggressive cancers. In addition to THC, there are many other cannabinoids found in CS, and a majority produces little to no psychoactivity due to the inability to activate cannabinoid receptors. For example, the second most abundant cannabinoid in CS is the non-psychoactive cannabidiol (CBD). Using animal models, CBD has been shown to inhibit the progression of many types of cancer including glioblastoma (GBM), breast, lung, prostate and colon cancer. This review will center on mechanisms by which CBD, and other plant-derived cannabinoids inefficient at activating cannabinoid receptors, inhibit tumor cell viability, invasion, metastasis, angiogenesis, and the stem-like potential of cancer cells. We will also discuss the ability of non-psychoactive cannabinoids to induce autophagy and apoptotic-mediated cancer cell death, and enhance the activity of first-line agents commonly used in cancer treatment. SN - 1557-1904 UR - https://www.unboundmedicine.com/medline/citation/25916739/The_Antitumor_Activity_of_Plant_Derived_Non_Psychoactive_Cannabinoids_ L2 - https://dx.doi.org/10.1007/s11481-015-9608-y DB - PRIME DP - Unbound Medicine ER -