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Molecular Cancer Therapeutics
Molecular Cancer Therapeutics
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Cannabidiol Enhances the Inhibitory Effects of Δ9-Tetrahydrocannabinol on Human Glioblastoma Cell Proliferation and Survival

Jahan P. Marcu, Rigel T. Christian, Darryl Lau, Anne J. Zielinski, Maxx P. Horowitz, Jasmine Lee, Arash Pakdel, Juanita Allison, Chandani Limbad, Dan H. Moore, Garret L. Yount, Pierre-Yves Desprez and Sean D. McAllister
Jahan P. Marcu
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Rigel T. Christian
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Darryl Lau
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Anne J. Zielinski
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Maxx P. Horowitz
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Jasmine Lee
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Arash Pakdel
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Juanita Allison
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Chandani Limbad
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Dan H. Moore
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Garret L. Yount
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Pierre-Yves Desprez
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Sean D. McAllister
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DOI: 10.1158/1535-7163.MCT-09-0407 Published January 2010
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Abstract

The cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptor agonist Δ9-tetrahydrocannabinol (THC) has been shown to be a broad-range inhibitor of cancer in culture and in vivo, and is currently being used in a clinical trial for the treatment of glioblastoma. It has been suggested that other plant-derived cannabinoids, which do not interact efficiently with CB1 and CB2 receptors, can modulate the actions of Δ9-THC. There are conflicting reports, however, as to what extent other cannabinoids can modulate Δ9-THC activity, and most importantly, it is not clear whether other cannabinoid compounds can either potentiate or inhibit the actions of Δ9-THC. We therefore tested cannabidiol, the second most abundant plant-derived cannabinoid, in combination with Δ9-THC. In the U251 and SF126 glioblastoma cell lines, Δ9-THC and cannabidiol acted synergistically to inhibit cell proliferation. The treatment of glioblastoma cells with both compounds led to significant modulations of the cell cycle and induction of reactive oxygen species and apoptosis as well as specific modulations of extracellular signal-regulated kinase and caspase activities. These specific changes were not observed with either compound individually, indicating that the signal transduction pathways affected by the combination treatment were unique. Our results suggest that the addition of cannabidiol to Δ9-THC may improve the overall effectiveness of Δ9-THC in the treatment of glioblastoma in cancer patients. Mol Cancer Ther; 9(1); 180–9

Keywords
  • cannabinoid
  • synergism
  • proliferation
  • invasion
  • apoptosis

Footnotes

  • Note: Supplementary material for this article is available at Molecular Cancer Therapeutics Online (http://mct.aacrjournals.org/).

    • Received May 11, 2009.
    • Revision received November 12, 2009.
    • Accepted November 15, 2009.
  • ©2010 American Association for Cancer Research.
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Molecular Cancer Therapeutics: 9 (1)
January 2010
Volume 9, Issue 1
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Cannabidiol Enhances the Inhibitory Effects of Δ9-Tetrahydrocannabinol on Human Glioblastoma Cell Proliferation and Survival
Jahan P. Marcu, Rigel T. Christian, Darryl Lau, Anne J. Zielinski, Maxx P. Horowitz, Jasmine Lee, Arash Pakdel, Juanita Allison, Chandani Limbad, Dan H. Moore, Garret L. Yount, Pierre-Yves Desprez and Sean D. McAllister
Mol Cancer Ther January 1 2010 (9) (1) 180-189; DOI: 10.1158/1535-7163.MCT-09-0407

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Cannabidiol Enhances the Inhibitory Effects of Δ9-Tetrahydrocannabinol on Human Glioblastoma Cell Proliferation and Survival
Jahan P. Marcu, Rigel T. Christian, Darryl Lau, Anne J. Zielinski, Maxx P. Horowitz, Jasmine Lee, Arash Pakdel, Juanita Allison, Chandani Limbad, Dan H. Moore, Garret L. Yount, Pierre-Yves Desprez and Sean D. McAllister
Mol Cancer Ther January 1 2010 (9) (1) 180-189; DOI: 10.1158/1535-7163.MCT-09-0407
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Molecular Cancer Therapeutics
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