The Inhibitory Effects of Cannabidiol on Systemic Malignant Tumors

The Inhibitory Effects of Cannabidiol on Systemic Malignant Tumors To the Editor: The recent article by Johnson et al. 1 provided for highly stimulating reading. Cannabidiol may attenuate tumor growth in a number of other systemic malignancies. Decreased tumor growth in pulmonary malignancies is seen after administration of cannabidiol. Cannabidiol increases the expression of cyclooxygenase-2 within the cancerous cells. 2 Cannabidiol also induces tissue inhibitor of metalloproteinase-1 synthesis and activity. Peroxisome proliferator-activated receptor-gamma expression is augmented at the same time. Intercellular adhesion molecule-1 induction also is seen typically. 3 As a result, intratumoral apoptosis is markedly accentuated. Cannabidiol also downregulates the expression of plasminogen activator inhibitor-1. 4 Increased nuclear translocation of peroxisome proliferator-activated receptor-gamma accompanies the above changes. Tumor metastasis also is markedly attenuated.</P>Similar attenuation of tumor growth is seen in breast malignancies. It mediates this antineoplastic effect by attenuating mammalian target of rapamycin signaling. 5 Endoplasmic reticulum stress is typically accentuated and the cytoplasmic release of cytochrome C is markedly enhanced. ID1 expression also is inhibited at the same time. 6 On the other hand, ID2 expression is markedly upregulated. AKT inhibition accompanies the above changes. As a consequence, there is both increased apoptosis and intratumoral autophagy. Interestingly, beclin-1 plays a major role in these changes.</P>The above examples clearly illustrate the significant antineoplastic effects of cannabidiol. Hopefully, the next few years will see increased studies to fully and further evaluate these antineoplastic effects.</P> http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Pain and Symptom Management Elsevier

The Inhibitory Effects of Cannabidiol on Systemic Malignant Tumors

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Publisher
Elsevier
Copyright
Copyright © 2013 U.S. Cancer Pain Relief Committee
ISSN
0885-3924
D.O.I.
10.1016/j.jpainsymman.2013.02.002
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Abstract

To the Editor: The recent article by Johnson et al. 1 provided for highly stimulating reading. Cannabidiol may attenuate tumor growth in a number of other systemic malignancies. Decreased tumor growth in pulmonary malignancies is seen after administration of cannabidiol. Cannabidiol increases the expression of cyclooxygenase-2 within the cancerous cells. 2 Cannabidiol also induces tissue inhibitor of metalloproteinase-1 synthesis and activity. Peroxisome proliferator-activated receptor-gamma expression is augmented at the same time. Intercellular adhesion molecule-1 induction also is seen typically. 3 As a result, intratumoral apoptosis is markedly accentuated. Cannabidiol also downregulates the expression of plasminogen activator inhibitor-1. 4 Increased nuclear translocation of peroxisome proliferator-activated receptor-gamma accompanies the above changes. Tumor metastasis also is markedly attenuated.</P>Similar attenuation of tumor growth is seen in breast malignancies. It mediates this antineoplastic effect by attenuating mammalian target of rapamycin signaling. 5 Endoplasmic reticulum stress is typically accentuated and the cytoplasmic release of cytochrome C is markedly enhanced. ID1 expression also is inhibited at the same time. 6 On the other hand, ID2 expression is markedly upregulated. AKT inhibition accompanies the above changes. As a consequence, there is both increased apoptosis and intratumoral autophagy. Interestingly, beclin-1 plays a major role in these changes.</P>The above examples clearly illustrate the significant antineoplastic effects of cannabidiol. Hopefully, the next few years will see increased studies to fully and further evaluate these antineoplastic effects.</P>

Journal

Journal of Pain and Symptom ManagementElsevier

Published: Apr 1, 2013

References

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