Regulation of inflammation and proliferation of human bladder carcinoma cells by type-1 and type-2 cannabinoid receptors.

“Pro-inflammatory cytokines, growth and angiogenic factors released by leukocytes are involved in carcinogenesis and cancer progression, but they are also crucial for fighting tumour growth and spreading.

We have previously demonstrated that endocannabinoids modulate cell-to-cell crosstalk during inflammation. Here, we investigated the inflammatory and tumourigenic properties of endocannabinoids in a human urinary bladdercarcinoma cell line…

Collectively, these findings suggest that CB receptors may play distinct roles in cancer biology, depending on the specific ligand employed.

CONCLUSIONS:

The in vivo assessment of the role of CB receptors in inflammation and cancer might be instrumental in broadening the understanding about bladder cancer biology.”

http://www.ncbi.nlm.nih.gov/pubmed/25445433

http://www.thctotalhealthcare.com/category/bladder-cancer/

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New insights into antimetastatic and antiangiogenic effects of cannabinoids.

“Cannabinoids exert antitumorigenic effects via multiple mechanisms.

Of these, antimetastatic and antiangiogenic actions have attracted considerable interest in the past years…

This chapter reviews the cell- and substance-specific antitumorigenic mechanisms of cannabinoids with particular consideration of their antimetastatic/anti-invasive and antiangiogenic actions.

In addition, beneficial interactions of cannabinoids with currently used chemotherapeutics as well as the influence of cannabinoids on tumor-immune surveillance are addressed.

Collectively, the currently available data suggest cannabinoids as a potential tool in modern cancer pharmacotherapy.”

http://www.ncbi.nlm.nih.gov/pubmed/25619715

http://www.thctotalhealthcare.com/category/cancer/

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Critical appraisal of the potential use of cannabinoids in cancer management

“Cannabinoids have been attracting a great deal of interest as potential anticancer agents. Originally derived from the plant Cannabis sativa, there are now a number of endo-, phyto- and synthetic cannabinoids available. This review summarizes the key literature to date around the actions, antitumor activity, and mechanisms of action for this broad range of compounds…

Two therapeutic avenues exist for the development of cannabinoids as anticancer agents. As antiemetic and analgesic compounds, this class of compounds has been explored in terms of palliative care. More recently, cannabinoid agonists and antagonists have been screened for potential direct antitumorigenic properties.

… results suggest that overall the cannabinoids affect multiple cellular signaling pathways, which means they have the potential to decrease cancer development, growth, and metastasis.

Overall, the cannabinoids may show future promise in the treatment of cancer, but there are many significant hurdles to be overcome. There is much still to be learned about the action of the cannabinoids and the endocannabinoid system.

It is a distinct possibility that the cannabinoids may have a place in the future treatment of cancer.”

Full Text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3770515/

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CYCLOOXYGENASE-2 AND PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR γ CONFER CANNABIDIOL-INDUCED APOPTOSIS OF HUMAN LUNG CANCER CELLS.

Abstract

“The antitumorigenic mechanism of cannabidiol (CBD) is still controversial. This study investigates the role of cyclooxygenase-2 (COX-2) and peroxisome proliferator activated receptor γ (PPARγ) in CBDs proapoptotic and tumor-regressive action. In lung cancer cell lines (A549, H460) and primary cells from a lung cancer patient CBD elicited decreased viability associated with apoptosis. Apoptotic cell death by CBD was suppressed by NS-398 (COX-2 inhibitor), GW-9662 (PPARγ antagonist) and siRNA targeting COX-2 and PPARγ. CBD-induced apoptosis was paralleled by upregulation of COX-2 and PPARγ mRNA and protein expression with a maximum induction of COX-2 mRNA after 8 h and continuous increases of PPARγ mRNA when compared to vehicle. In response to CBD tumor cell lines exhibited increased levels of COX-2-dependent prostaglandins (PGs) among which PGD2 and 15-deoxy-Δ12,14-PGJ2 (15d-PGJ2) caused a translocation of PPARγ to the nucleus and induced a PPARγ-dependent apoptotic cell death. Moreover, in A549-xenografted nude mice CBD caused upregulation of COX-2 and PPARγ in tumor tissue, and tumor regression that was fully reversible by GW-9662. Together, our data demonstrate a novel proapoptotic mechanism of CBD involving initial upregulation of COX-2 and PPARγ and a subsequent nuclear translocation of PPARγ by COX-2-dependent PGs.”

http://www.ncbi.nlm.nih.gov/pubmed/23220503

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