Cancer is not a sentence. CBD is an ally in the fight against cancer.

by in About CBD 4 March 2019

We do not have a cure for cancer. Every year, cancer kills about 8 million people. Although diagnosing cancer does not itself mean the end, it means the beginning of the fight. Fights that are hard to win though there are those who succeed.

What is cancer? It is a collection of cells with impaired proliferation, i.e. showing excessive multiplication. These cells, by mutation in DNA, do not stop dividing, which is why they form tumors. It is unimaginable that although a human consists of trillions (!) of cells, it is enough that one has a mutation to develop a cancer. Why is fighting cancer so difficult? Firstly because it is not a foreign cell in our body but our own – although mutated. The immune system in this case can not distinguish the enemy. Cancer is camouflaging in our body. It can not always be cut. It can be metastasized to other organs or not be noticed for many years. In addition, the tumor originating from one tissue is completely different from the tumor originating from another tissue. This is a totally different disease entity. Chemotherapy, though considered by many to be a golden mean, really consists in killing cells that divide quickly, including healthy ones.

We do not have a cure for cancer. However, we keep looking for it because, although we can not always stop it, we can often slow down its development. When confronting various substances with cancer, we finally put cannabidiol on their path. It’s time to look at the research.


CBD in the fight against cancer

As we have already written, every cancer is actually a completely different disease entity. Therefore, we can not simultaneously examine the effect of cannabidiol on all types and types of cancer. We can, however, consistently study the impact of CBD on each cancer separately. Although this is a difficult process, the first results seem to be very positive. We would like to introduce you to a few of them.


CBD in the fight against the brain tumor

Evidence suggests that cannabidiol has antitumor activity in many types of cancer, including glioblastoma multiforme (GBM). Glioma is a malignant brain tumor of glial origin. The effects of CBD have been studied in monotherapy and in combination with cytostatics in several human GBM cell lines and in primary mouse GBM cells. Cannabidiol has been shown to have antitumor activity in many GBM cell lines [1-9]. This antitumor activity is mediated by the cell membrane-associated receptors, including the GPR55 receptor and the TRPV receptor, and involves the production of reactive oxygen as well as the induction of autophagy and apoptosis [10-17]. Interestingly, recent studies have reported that antitumor activity of CBD interacts with the activity of cytostatics suggesting that combination regimens may bring greater benefits to patients diagnosed with GBM [18], but this study reported activity in one human GBM cell line (U87MG ) [19]. Thus, a more detailed and quantitative assessment of the CBD-induced responses (and associated with it in cytostatics therapy) is required for a better understanding of the therapeutic potential of CBD in the treatment of GBM.


CBD in the fight against breast and nipple cancer

The antitumor activity of CBD against highly aggressive breast and nipple cancer cell lines, including the TNBC subtype, or triply negative, was examined. CBD significantly inhibits proliferation induced by epidermal growth factor (EGF) and chemotaxis of nipple cancer cells. Further studies have shown that CBD inhibits EGF-induced activation of the EGFR signaling pathways, ERK, AKT and NF-kB, as well as the secretion of MMP2 and MMP9. In addition, CBD has been shown to inhibit tumor growth and metastasis in various mouse model systems. Analysis of molecular mechanisms has shown that CBD significantly inhibits the recruitment of tumor-associated macrophages in the primary tumor stroma and secondary lung metastases. CBD inhibits the growth and metastasis of breast cancer through new mechanisms by inhibiting EGF / EGFR signaling and modulating the tumor microenvironment.

These results indicate that CBD can be used as a new therapeutic option to inhibit the growth and metastasis of highly aggressive subtypes of nipple cancer, including TNBC, which currently have limited therapeutic options and are associated with poor prognosis and low survival rates [20].

CBD in the fight against cervical cancer

To test the effect of CBD on cancer cells of cervical cancer, phytochemical screening, MTT, cell growth analysis, flow cytometry, morphological analysis, Western blotting, caspase assay and ATP measurement test were performed.

The results obtained indicate that both cannabidiol and Cannabis sativa extracts were able to inhibit cell proliferation in all cell lines at various concentrations. In addition, apoptosis was induced by cannabidiol, as demonstrated by increased subGO / G1 and apoptosis by annexin V. Apoptosis was confirmed by overexpression of p53, caspase 3 and bax. Induction of apoptosis was additionally confirmed by morphological changes, increase in caspase 3/7 and decrease in ATP level [21].

The results above indicate the relative efficacy of inhibition of cervical tumor growth by cannabidiol. Thus, the CBD has demonstrated its activity on many levels of fight against the growth factors of several cancers. There is still a lot of work and a lot of research ahead of us, but the results so far have been optimistic. Can cannabidiol be helpful in the fight against cancer? For now, everything indicates it can.


References and research used in the article:

  1.    Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines. Massi P, Vaccani A, Ceruti S, Colombo A, Abbracchio MP, Parolaro D. J Pharmacol Exp Ther. 2004 Mar; 308(3):838-45.
  2.        The non-psychoactive cannabidiol triggers caspase activation and oxidative stress in human glioma cells. Massi P, Vaccani A, Bianchessi S, Costa B, Macchi P, Parolaro D. Cell Mol Life Sci. 2006 Sep; 63(17):2057-66.
  3.       5-Lipoxygenase and anandamide hydrolase (FAAH) mediate the antitumor activity of cannabidiol, a non-psychoactive cannabinoid. Massi P, Valenti M, Vaccani A, Gasperi V, Perletti G, Marras E, Fezza F, Maccarrone M, Parolaro D. J Neurochem. 2008 Feb; 104(4):1091-100.
  4.       Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor-independent mechanism. Vaccani A, Massi P, Colombo A, Rubino T, Parolaro D. Br J Pharmacol. 2005 Apr; 144(8):1032-6.
  5.       Cannabidiol enhances the inhibitory effects of delta9-tetrahydrocannabinol on human glioblastoma cell proliferation and survival. Marcu JP, Christian RT, Lau D, Zielinski AJ, Horowitz MP, Lee J, Pakdel A, Allison J, Limbad C, Moore DH, Yount GL, Desprez PY, McAllister SD. Mol Cancer Ther. 2010 Jan; 9(1):180-9.
  6.       A combined preclinical therapy of cannabinoids and temozolomide against glioma. Torres S, Lorente M, Rodríguez-Fornés F, Hernández-Tiedra S, Salazar M, García-Taboada E, Barcia J, Guzmán M, Velasco G. Mol Cancer Ther. 2011 Jan; 10(1):90-103.
  7.       Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents. Nabissi M, Morelli MB, Santoni M, Santoni G. Carcinogenesis. 2013 Jan; 34(1):48-57.
  8.       Cannabidiol, a non-psychoactive cannabinoid compound, inhibits proliferation and invasion in U87-MG and T98G glioma cells through a multitarget effect. Solinas M, Massi P, Cinquina V, Valenti M, Bolognini D, Gariboldi M, Monti E, Rubino T, Parolaro D. PLoS One. 2013; 8(10):e76918.
  9.       Id-1 is a key transcriptional regulator of glioblastoma aggressiveness and a novel therapeutic target. Soroceanu L, Murase R, Limbad C, Singer E, Allison J, Adrados I, Kawamura R, Pakdel A, Fukuyo Y, Nguyen D, Khan S, Arauz R, Yount GL, Moore DH, Desprez PY, McAllister SD. Cancer Res. 2013 Mar 1; 73(5):1559-69.
  10.      Molecular targets for cannabidiol and its synthetic analogues: effect on vanilloid VR1 receptors and on the cellular uptake and enzymatic hydrolysis of anandamide. Bisogno T, Hanus L, De Petrocellis L, Tchilibon S, Ponde DE, Brandi I, Moriello AS, Davis JB, Mechoulam R, Di Marzo V. Br J Pharmacol. 2001 Oct; 134(4):845-52.
  11.    Antitumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma. Ligresti A, Moriello AS, Starowicz K, Matias I, Pisanti S, De Petrocellis L, Laezza C, Portella G, Bifulco M, Di Marzo V. J Pharmacol Exp Ther. 2006 Sep; 318(3):1375-87.
  12.    The non-psychoactive cannabidiol triggers caspase activation and oxidative stress in human glioma cells. Massi P, Vaccani A, Bianchessi S, Costa B, Macchi P, Parolaro D. Cell Mol Life Sci. 2006 Sep; 63(17):2057-66.
  13. A role for L-alpha-lysophosphatidylinositol and GPR55 in the modulation of migration, orientation and polarization of human breast cancer cells. Ford LA, Roelofs AJ, Anavi-Goffer S, Mowat L, Simpson DG, Irving AJ, Rogers MJ, Rajnicek AM, Ross R.Br J Pharmacol. 2010 Jun; 160(3):762-71.
  14. Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1. Ramer R, Merkord J, Rohde H, Hinz B. Biochem Pharmacol. 2010 Apr 1; 79(7):955-66.
  15. TRPV2 activation induces apoptotic cell death in human T24 bladder cancer cells: a potential therapeutic target for bladder cancer. Yamada T, Ueda T, Shibata Y, Ikegami Y, Saito M, Ishida Y, Ugawa S, Kohri K, Shimada S. Urology. 2010 Aug; 76(2):509.e1-7.
  16.    The putative cannabinoid receptor GPR55 defines a novel autocrine loop in cancer cell proliferation. Piñeiro R, Maffucci T, Falasca M. Oncogene. 2011 Jan 13; 30(2):142-52.
  17.    Modulation of L-α-lysophosphatidylinositol/GPR55 mitogen-activated protein kinase (MAPK) signaling by cannabinoids. Anavi-Goffer S, Baillie G, Irving AJ, Gertsch J, Greig IR, Pertwee RG, Ross RA. J Biol Chem. 2012 Jan 2; 287(1):91-104.
  18.    . Quantitative Analyses of Synergistic Responses between Cannabidiol and DNA-Damaging Agents on the Proliferation and Viability of Glioblastoma and Neural Progenitor Cells in Culture. Liting Deng, Lindsay Ng, Tatsuya Ozawa and Nephi Stellacorresponding
  19. Triggering of the TRPV2 channel by cannabidiol sensitizes glioblastoma cells to cytotoxic chemotherapeutic agents. Nabissi M, Morelli MB, Santoni M, Santoni G. Carcinogenesis. 2013 Jan; 34(1):48-57.
  20.    Modulation of the tumor microenvironment and inhibition of EGF/EGFR pathway: Novel anti‐tumor mechanisms of Cannabidiol in breast cancer. Mohamad Elbaz, Mohd W. Nasser, Janani Ravi, Nissar A. Wani, Dinesh K. Ahirwar, Helong Zhao, Steve Oghumu, Abhay R. Satoskar, Konstantin Shilo, William E. Carson and Ramesh K.
  21.    Cannabidiol rather than Cannabis sativa extracts inhibit cell growth and induce apoptosis in cervical cancer cells. Sindiswa T. Lukhele and Lesetja R.


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