• Corpus ID: 4842915

Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor.

@article{Snchez2001InhibitionOG,
  title={Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor.},
  author={Cristina S{\'a}nchez and Mar{\'i}a L. de Ceballos and Teresa G{\'o}mez del Pulgar and Daniel Rueda and C{\'e}sar Corbacho and Guillermo Velasco and Ismael Galve-Roperh and John W Huffman and Santiago Ram{\'o}n y. Cajal and Manuel Guzm{\'a}n},
  journal={Cancer research},
  year={2001},
  volume={61 15},
  pages={
          5784-9
        }
}
The development of new therapeutic strategies is essential for the management of gliomas, one of the most malignant forms of cancer. We have shown previously that the growth of the rat glioma C6 cell line is inhibited by psychoactive cannabinoids (I. Galve-Roperh et al., Nat. Med., 6: 313-319, 2000). These compounds act on the brain and some other organs through the widely expressed CB(1) receptor. By contrast, the other cannabinoid receptor subtype, the CB(2) receptor, shows a much more… 

Figures and Tables from this paper

Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors.

It is shown that the CB(1) and theCB(2) receptor are expressed in normal skin and skin tumors of mice and humans and support a new therapeutic approach for the treatment of skin tumors.

Arachidonylethanolamide Induces Apoptosis of Human Glioma Cells through Vanilloid Receptor‐1

It is observed that AEA induced apoptosis in long-term and recently established glioma cell lines via aberrantly expressed vanilloid receptor-1 (VR1), which shows that the selective targeting of VR1 by AEA or more stable analogues is an attractive research area for the treatment of gliomas.

Synthetic Cannabinoids Influence the Invasion of Glioblastoma Cell Lines in a Cell- and Receptor-Dependent Manner

Cannabinoids can influence glioblastoma cell invasion in a receptor and cell type specific manner that is independent of proliferation and apoptosis, and can potentially be used in the future as an addition to current therapy.

Cannabinoids inhibit glioma cell invasion by down-regulating matrix metalloproteinase-2 expression.

Manipulation of MMP-2 expression by RNA interference and cDNA overexpression experiments proved that down-regulation of this MMP plays a critical role in THC-mediated inhibition of cell invasion and constitutes a new hallmark of cannabinoid antitumoral activity.

Evaluation of anti-invasion effect of cannabinoids on human hepatocarcinoma cells

Investigation of the potential antitumoral and anti-invasive activity of cannabinoids on HepG2 cells and the possible roles of matrix metalloproteinase-2 (MMP-2) and MMP-9 in its action revealed that both cannabinoids reduce cell viability, cell invasion and expression in higher dose of 20 nM.

Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease.

The current data demonstrate that CB2 cannabinoid receptors expressed on malignancies of the immune system may serve as potential targets for the induction of apoptosis, and because CB2 agonists lack psychotropic effects, they may Serve as novel anticancer agents to selectively target and kill tumors of immune origin.

Endocannabinoid signaling in glioma.

Increasing basic knowledge on how (endo)cannabinoids act on glioma cells could help to optimize experimental cannabinoid-based anti-tumoral therapies, as well as the preliminary clinical testing that is currently underway.

Cannabinoids and Gliomas

The good safety profile of THC, together with its possible growth-inhibiting action on tumor cells, justifies the setting up of future trials aimed at evaluating the potential antitumoral activity of cannabinoids.

Mechanism of anti-glioma activity and in vivo efficacy of the cannabinoid ligand KM-233

Findings indicate that structural refinement of KM-233 to improve its biopharmaceutical properties may lead to a novel and efficacious treatment for GBM.

Selective, nontoxic CB(2) cannabinoid o-quinone with in vivo activity against triple-negative breast cancer.

Triple-negative breast cancer (TNBC) represents a subtype of breast cancer characterized by high aggressiveness. There is no current targeted therapy for these patients whose prognosis, as a group,
...

References

SHOWING 1-10 OF 50 REFERENCES

Control of the cell survival/death decision by cannabinoids

The neuroprotective effect of cannabinoids may have potential clinical relevance for the treatment of neurodegenerative disorders such as multiple sclerosis, Parkinson's disease, and ischemia/stroke, whereas their growth-inhibiting action on transformed cells might be useful for the management of malignant brain tumors.

The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation.

The data suggest that anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous Prolactin action at the level of prolactin receptor.

Anti-tumoral action of cannabinoids: Involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation

It is shown that intratumoral administration of Δ9-tetrahydrocannabinol and the synthetic cannabinoid agonist WIN-55,212-2 induced a considerable regression of malignant gliomas in Wistar rats and in mice deficient in recombination activating gene 2.

HU-308: a specific agonist for CB(2), a peripheral cannabinoid receptor.

  • L. HanušA. Breuer E. Fride
  • Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1999
HU-308 reduces blood pressure, blocks defecation, and elicits anti-inflammatory and peripheral analgesic activity, demonstrating the feasibility of discovering novel nonpsychotropic cannabinoids that may lead to new therapies for hypertension, inflammation, and pain.

Evaluation of binding in a transfected cell line expressing a peripheral cannabinoid receptor (CB2): identification of cannabinoid receptor subtype selective ligands.

Although most of the chosen compounds did not discriminate between CB1 and CB2, several ligands were identified that showed selectivity and can now serve as a basis for the design of compounds with even greater selectivity.

Δ-9-Tetrahydrocannabinol Inhibits Antitumor Immunity by a CB2 Receptor-Mediated, Cytokine-Dependent Pathway1

It is shown that Δ-9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, suppresses host immune reactivity against lung cancer and promotes tumor growth by inhibiting antitumor immunity by a CB2 receptor-mediated, cytokine-dependent pathway.

Synergistic cytotoxicity in solid tumor cell lines between N-(4-hydroxyphenyl)retinamide and modulators of ceramide metabolism.

Combinations of 4-HPR and modulators of ceramide metabolism may form the basis for a novel chemotherapy that is functional under hypoxic conditions (e.g., such as those within tumors) and is p53 independent and caspase independent.

SR 144528, the first potent and selective antagonist of the CB2 cannabinoid receptor.

It is expected that SR 144528 will provide a powerful tool to investigate the in vivo functions of the cannabinoid system in the immune response.

Molecular characterization of a peripheral receptor for cannabinoids

The cloning of a receptor for cannabinoids is reported that is not expressed in the brain but rather in macrophages in the marginal zone of spleen, which helps clarify the non-psychoactive effects of cannabinoids.

Structure of a cannabinoid receptor and functional expression of the cloned cDNA

The cloning and expression of a complementary DNA that encodes a G protein-coupled receptor that is involved in cannabinoid-induced CNS effects (including alterations in mood and cognition) experienced by users of marijuana are suggested.