Cannabidiol (CBD) as a Promising Anti-Cancer Drug

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Abstract

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The use of cannabinoids containing plant extracts as herbal medicine can be traced back to as early as 500 BC. In recent years, the medical and health-related applications of one of the non-psychotic cannabinoids, cannabidiol or CBD, has garnered tremendous attention. In this review, we will discuss the most recent findings that strongly support the further development of CBD as a promising anti-cancer drug.

Abstract

Recently, cannabinoids, such as cannabidiol (CBD) and Δ ⁹-tetrahydrocannabinol (THC), have been the subject of intensive research and heavy scrutiny. Cannabinoids encompass a wide array of organic molecules, including those that are physiologically produced in humans, synthesized in laboratories, and extracted primarily from the Cannabis sativa plant. These organic molecules share similarities in their chemical structures as well as in their protein binding profiles. However, pronounced differences do exist in their mechanisms of action and clinical applications, which will be briefly compared and contrasted in this review. The mechanism of action of CBD and its potential applications in cancer therapy will be the major focus of this review article.

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Most cited references 134

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Cancer-related inflammation.

Alberto Mantovani, Paola Allavena, Antonio Sica … (2008)

The mediators and cellular effectors of inflammation are important constituents of the local environment of tumours. In some types of cancer, inflammatory conditions are present before a malignant change occurs. Conversely, in other types of cancer, an oncogenic change induces an inflammatory microenvironment that promotes the development of tumours. Regardless of its origin, 'smouldering' inflammation in the tumour microenvironment has many tumour-promoting effects. It aids in the proliferation and survival of malignant cells, promotes angiogenesis and metastasis, subverts adaptive immune responses, and alters responses to hormones and chemotherapeutic agents. The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.

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Molecular characterization of a peripheral receptor for cannabinoids.

S. MUNRO, K L Thomas, M. Abu-Shaar … (1993)

The major active ingredient of marijuana, delta 9-tetrahydrocannabinol (delta 9-THC), has been used as a psychoactive agent for thousands of years. Marijuana, and delta 9-THC, also exert a wide range of other effects including analgesia, anti-inflammation, immunosuppression, anticonvulsion, alleviation of intraocular pressure in glaucoma, and attenuation of vomiting. The clinical application of cannabinoids has, however, been limited by their psychoactive effects, and this has led to interest in the biochemical bases of their action. Progress stemmed initially from the synthesis of potent derivatives of delta 9-THC, and more recently from the cloning of a gene encoding a G-protein-coupled receptor for cannabinoids. This receptor is expressed in the brain but not in the periphery, except for a low level in testes. It has been proposed that the nonpsychoactive effects of cannabinoids are either mediated centrally or through direct interaction with other, non-receptor proteins. Here we report the cloning of a receptor for cannabinoids that is not expressed in the brain but rather in macrophages in the marginal zone of spleen.

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Activation of apoptosis signalling pathways by reactive oxygen species.

Maureen Redza-Dutordoir, Diana Averill-Bates (2016)

Reactive oxygen species (ROS) are short-lived and highly reactive molecules. The generation of ROS in cells exists in equilibrium with a variety of antioxidant defences. At low to modest doses, ROS are considered to be essential for regulation of normal physiological functions involved in development such as cell cycle progression and proliferation, differentiation, migration and cell death. ROS also play an important role in the immune system, maintenance of the redox balance and have been implicated in activation of various cellular signalling pathways. Excess cellular levels of ROS cause damage to proteins, nucleic acids, lipids, membranes and organelles, which can lead to activation of cell death processes such as apoptosis. Apoptosis is a highly regulated process that is essential for the development and survival of multicellular organisms. These organisms often need to discard cells that are superfluous or potentially harmful, having accumulated mutations or become infected by pathogens. Apoptosis features a characteristic set of morphological and biochemical features whereby cells undergo a cascade of self-destruction. Thus, proper regulation of apoptosis is essential for maintaining normal cellular homeostasis. ROS play a central role in cell signalling as well as in regulation of the main pathways of apoptosis mediated by mitochondria, death receptors and the endoplasmic reticulum (ER). This review focuses on current understanding of the role of ROS in each of these three main pathways of apoptosis. The role of ROS in the complex interplay and crosstalk between these different signalling pathways remains to be further unravelled during the coming years.

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Author and article information

Journal

Journal ID (nlm-ta): Cancers (Basel)

Journal ID (iso-abbrev): Cancers (Basel)

Journal ID (publisher-id): cancers

Title: Cancers

Publisher: MDPI

ISSN (Electronic): 2072-6694

Publication date (Electronic): 30 October 2020

Publication date Collection: November 2020

Volume: 12

Issue: 11

Electronic Location Identifier: 3203

Affiliations

[1 ]Department of Biomedical Sciences, College of Osteopathic Medicine, New York Institute of Technology, Old Westbury, NY 11568, USA; eseltz01@ 123456nyit.edu (E.S.S.); awatters@ 123456nyit.edu (A.K.W.); dmackenz@ 123456nyit.edu (D.M.J.)

[2 ]Department of Internal Medicine, Cleveland Clinic, Cleveland, OH 44195, USA; GranatL2@ 123456ccf.org

Author notes

[* ]Correspondence: dzhang12@ 123456nyit.edu ; Tel.: +1-516-686-3872; Fax: +1-516-686-3832

[†]

These authors contributed to this paper equally.

Author information

Emily S. Seltzer https://orcid.org/0000-0002-5404-424X

Andrea K. Watters https://orcid.org/0000-0003-3810-0675

Danny MacKenzie Jr. https://orcid.org/0000-0002-3632-6040

Lauren M. Granat https://orcid.org/0000-0001-8362-5492

Dong Zhang https://orcid.org/0000-0002-4515-2070

Article

Publisher ID: cancers-12-03203

DOI: 10.3390/cancers12113203

PMC ID: 7693730

PubMed ID: 33143283

SO-VID: 6805144f-e45f-44b0-aad9-cfe11647a8a3

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Cannabidiol (CBD) as a Promising Anti-Cancer Drug

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Abstract

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Anti-Trafficking Review

Most cited references 134

Cancer-related inflammation.

Molecular characterization of a peripheral receptor for cannabinoids.

Activation of apoptosis signalling pathways by reactive oxygen species.

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