Hypoxia-induced inhibition of the endocannabinoid system in glioblastoma cells.

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“The endocannabinoid system plays an important role in the regulation of physiological and pathological conditions, including inflammation and cancer.

Hypoxia is a fundamental phenomenon for the establishment and maintenance of the microenvironments in various physiological and pathological conditions. However, the influence of hypoxia on the endocannabinoid system is not fully understood. In the present study, we investigated the effects of hypoxia on the endocannabinoid system in malignant brain tumors.

Although cannabinoid receptor (CB) engagement induces cell death in U-87 MG cells in normoxic conditions, CB agonist-induced death was attenuated in hypoxic conditions. These results suggest that hypoxia modifies the endocannabinoid system in glioblastoma cells.

Hypoxia-induced inhibition of the endocannabinoid system may aid the development of glioblastoma.”


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The Synthetic Cannabinoid WIN 55,212-2 Elicits Death in Human Cancer Cell Lines.

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“Studies have revealed that cancer might be treated with cannabinoids since they can influence cancer cell survival. These findings suggest an alternative treatment option to chemo- and radiotherapy, that are associated with numerous adverse side-effects for the patients.


Viability staining was conducted on lung cancer, testicular cancer and neuroblastoma cells treated with different concentrations of the synthetic cannabinoid WIN 55,212-2 and the percentage of dead cells was compared. Activity of apoptosis-related enzymes was investigated by the presence of DNA ladder in gel electrophoresis.


Treatment with different WIN 55,212-2 concentrations led to a significant dose-dependent reduction of cell viability. A DNA ladder was observed after WIN 55,212-2 treatment of testicular cancer and lung cancer cells.


The application of WIN 55,212-2 was found to trigger cell death in the investigated cell lines. The decline in lung cancer and testicular cancer cell viability seems to have been caused by apoptosis. These findings may contribute to development of alternative cancer therapy strategies.”


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Synergistic interaction of the cannabinoid and death receptor systems: A potential target for future cancer therapies?

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“Cannabinoid receptors have been shown to interact with other receptors, including Tumor Necrosis Factor Receptor Superfamily (TNFRS) members, to induce cancer cell death. When cannabinoids and death-inducing ligands (including TRAIL) are administered together, they have been shown to synergize and demonstrate enhanced antitumor activity in vitro. Certain cannabinoid ligands have been shown to sensitize cancer cells and synergistically interact with members of the TNFRS, thus suggesting that the combination of cannabinoids with death receptor (DR) ligands induces additive or synergistic tumor cell death. This review summarizes recent findings on the interaction of the cannabinoid and DR systems and suggests possible clinical co-application of cannabinoids and DR ligands in the treatment of various malignancies.”



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Regulation of human glioblastoma cell death by combined treatment of cannabidiol, γ-radiation and small molecule inhibitors of cell signaling pathways.

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“Glioblastoma (GBM) is the most common primary malignant brain tumor in adults. The challenging problem in cancer treatment is to find a way to upregulate radiosensitivity of GBM while protecting neurons and neural stem/progenitor cells in the brain. The goal of the present study was upregulation of the cytotoxic effect of γ-irradiation in GBM by non-psychotropic and non-toxic cannabinoid, cannabidiol (CBD).

We emphasized three main aspects of signaling mechanisms induced by CBD treatment (alone or in combination with γ-irradiation) in human GBM that govern cell death: 1) CBD significantly upregulated the active (phosphorylated) JNK1/2 and MAPK p38 levels with the subsequent downregulation of the active phospho-ERK1/2 and phospho-AKT1 levels. MAPK p38 was one of the main drivers of CBD-induced cell death, while death levels after combined treatment of CBD and radiation were dependent on both MAPK p38 and JNK. Both MAPK p38 and JNK regulate the endogenous TRAIL expression. 2) NF-κB p65-P(Ser536) was not the main target of CBD treatment and this transcription factor was found at high levels in CBD-treated GBM cells. Additional suppression of p65-P(Ser536) levels using specific small molecule inhibitors significantly increased CBD-induced apoptosis. 3) CBD treatment substantially upregulated TNF/TNFR1 and TRAIL/TRAIL-R2 signaling by modulation of both ligand and receptor levels followed by apoptosis.

Our results demonstrate that radiation-induced death in GBM could be enhanced by CBD-mediated signaling in concert with its marginal effects for neural stem/progenitor cells and astrocytes. It will allow selecting efficient targets for sensitization of GBM and overcoming cancer therapy-induced severe adverse sequelae.”

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Endocannabinoids modulate apoptosis in endometriosis and adenomyosis.

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“Adenomyosis that is a form of endometriosis is the growth of ectopic endometrial tissue within the muscular wall of the uterus (myometrium), which may cause dysmenorrhea and infertility. Endocannabinoid mediated apoptotic mechanisms of endometriosis and adenomyosis are not known. We hypothesized that the down regulation of endocannabinoid receptors and/or alteration in their regulatory enzymes may have a direct role in the pathogenesis of endometriosis and adenomyosis through apoptosis.

Endocannabinoid receptors CB1 and CB2, their synthesizing and catabolizing enzymes (FAAH, NAPE-PLD, DAGL, MAGL) and the apoptotic indexes were immunohistochemically assessed in endometriotic and adenomyotic tissues. Findings were compared to normal endometrium and myometrium. Endometrial adenocarcinoma (Ishikawa) and ovarian endometriosis cyst wall stromal (CRL-7566) cell lines were furthermore cultured with or without cannabinoid receptor agonists. The IC50 value for CB1 and CB2 receptor agonists was quantified. Cannabinoid agonists on cell death were investigated by Annexin-V/Propidium iodide labeling with flow cytometry. CB1 and CB2 receptor levels decreased in endometriotic and adenomyotic tissues compared to the control group (p=0,001 and p=0,001). FAAH, NAPE-PLD, MAGL and DAGL enzyme levels decreased in endometriotic and adenomyotic tissues compared to control (p=0,001, p=0,001, p=0,001 and p=0,002 respectively). Apoptotic cell indexes both in endometriotic and adenomyotic tissues also decreased significantly, compared to the control group (p=0,001 and p=0,001). CB1 and CB2 receptor agonist mediated dose dependent fast anti-proliferative and pro-apoptotic effects were detected in Ishikawa and ovarian endometriosis cyst wall stromal cell lines (CRL-7566).

Endocannabinoids are suggested to increase apoptosis mechanisms in endometriosis and adenomyosis. CB1 and CB2 antagonists can be considered as potential medical therapeutic agents for endometriosis and adenomyosis.”



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Genetic or pharmacological depletion of cannabinoid CB1 receptor protects against dopaminergic neurotoxicity induced by methamphetamine in mice.


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“Accumulating evidence suggests that cannabinoid ligands play delicate roles in cell survival and apoptosis decisions, and that cannabinoid CB1 receptors (CB1R) modulate dopaminergic function.

However, the role of CB1R in methamphetamine (MA)-induced dopaminergic neurotoxicity in vivo remains elusive.

Multiple high doses of MA increased phospho-ERK and CB1R mRNA expressions in the striatum of CB1R (+/+) mice. These increases were attenuated by CB1R antagonists (i.e., AM251 and rimonabant), an ERK inhibitor (U0126), or dopamine D2R antagonist (sulpiride).

CB1R agonist-induced toxic effects were significantly attenuated by CB1R knockout, CB1R antagonists or PKCδ knockout.

Therefore, our results suggest that interaction between D2R, ERK and CB1R is critical for MA-induced dopaminergic neurotoxicity and that PKCδ mediates dopaminergic damage induced by high-doses of CB1R agonist.”


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It’s Colorectal Cancer Awareness Month. Please Be Aware:

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 “Prevention and Treatment of Colorectal Cancer by Natural Agents From Mother Nature. This review clearly demonstrates that various nutraceuticals provided by the Mother Nature have a huge potential for both prevention and treatment of Colorectal cancer (CRC). Since these agents can be administered chronically without any concern for safety and are highly affordable, their use has been the wave of the past and is likely to continue as the wave of the future.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3693477/
“Links between inflammation and colon cancer metastasis” https://www.sciencedaily.com/releases/2015/08/150825094923.htm
“Inflammation and colon cancer. The connection between inflammation and tumorigenesis is well-established. Inflammation is also likely to be involved with other forms of sporadic as well as heritable colon cancer.https://www.ncbi.nlm.nih.gov/pubmed/20420949
“Cannabis-derived substances in cancer therapy–an emerging anti-inflammatory role for the cannabinoids. Chronic inflammation has been associated with neoplasia for sometime, and as a consequence, reducing inflammation as a way of impacting cancer presents a new role for these compounds. https://www.ncbi.nlm.nih.gov/pubmed/20925645
“Cannabinoids as gastrointestinal anti-inflammatory drugs.” https://www.ncbi.nlm.nih.gov/pubmed/28239924
“Colon Cancer Risk Linked To High-Fat Diet: How Eating More Fat Can Increase Intestinal Tumors” http://www.medicaldaily.com/colon-cancer-high-fat-diet-intestinal-tumors-376664
“Study: Red and Processed Meats Linked With Colon Cancer Risk” http://healthland.time.com/2011/05/27/study-red-and-processed-meats-linked-with-colon-cancer-risk/
“Eating hot dogs, ham and other processed meat can cause colorectal cancer, and eating red meat “probably” can cause cancer, the World Health Organization’s cancer agency reported” http://www.usatoday.com/story/news/nation/2015/10/26/experts-processed-meats-can-cause-cancer/74615390/
“Mediterranean Diet Reduces Risk of Colon Cancer”
“More evidence a veg diet might lower cancer risk” http://www.today.com/health/veggie-diet-lowers-colon-cancer-risk-t7671
“Omegas linked with colon cancer survival. A large, observational study has linked higher intake of omega-3s with a lower risk of dying from colon cancer.” http://www.newhope.com/breaking-news/omegas-linked-colon-cancer-survival
 “Study shows how high-fat diets increase colon cancer risk” http://news.temple.edu/news/2012-03-06/study-shows-how-high-fat-diets-increase-colon-cancer-risk
“Poor metabolic health linked to increased risk for colorectal cancer in normal-weight women” http://www.news-medical.net/news/20170201/Poor-metabolic-health-linked-to-increased-risk-for-colorectal-cancer-in-normal-weight-women.aspx
“Cheese, Milk, and Fatty Fish Can Help Fight Colon Cancer” https://munchies.vice.com/en_us/article/cheese-milk-and-fatty-fish-can-help-fight-colon-cancer
“Diet, exercise and aspirin: 3 tools to fight colon cancer” http://ktar.com/story/1314810/diet-exercise-aspirin-3-tools-fight-colon-cancer/
“Many Early Colon Cancers Linked to Inherited Genes” https://medlineplus.gov/news/fullstory_162574.html
“E.coli Bacteria Linked to Colon Cancer” http://www.ibtimes.co.uk/e-coli-bateria-linked-colon-cancer-375102
“Colorectal cancer prevalence linked to human papillomavirus: a systematic review with meta-analysis” http://www.scielo.br/scielo.php?pid=S1415-790X2016000400791&script=sci_arttext&tlng=en
“Colon cancer linked to viruses in beef, Nobel-winning scientist contends” http://www.scmp.com/lifestyle/health/article/1695757/colon-cancer-linked-viruses-beef-nobel-winning-scientist-contends
“Diet High in Choline Linked with Increased Risk of Colorectal Polyps. According to the results of a study published in the Journal of the National Cancer Institute, high intake of choline-a nutrient found in foods such as red meat, eggs, poultry, and dairy products-may be linked with an increased risk of colorectal polyps.” http://news.cancerconnect.com/diet-high-in-choline-linked-with-increased-risk-of-colorectal-polyps/
“High-Glycemic Foods Linked to Colon Cancer. These foods include breads, pastas, pancakes, and other carbohydrates made from refined “white” grains, as well as other processed or sugary foods such as cakes, cookies, and other snacks.” http://www.webmd.com/colorectal-cancer/news/20040203/high-glycemic-foods-linked-to-colon-cancer#1
“Low-carb diet cuts risk of colon cancer” https://www.utoronto.ca/news/low-carb-diet-cuts-risk-colon-cancer
“Common food additive promotes colon cancer in mice. Emulsifiers, which are added to most processed foods to aid texture and extend shelf life, can alter intestinal bacteria in a manner that promotes intestinal inflammation and colorectal cancer” https://www.sciencedaily.com/releases/2016/11/161107110639.htm
“Processed meats including bacon, hot dogs linked to colon cancer” http://www.cp24.com/news/processed-meats-including-bacon-hot-dogs-linked-to-colon-cancer-1.2627498
“Processed meat can cause colon cancer, World Health Organization says” http://www.cbc.ca/news/health/meat-cancer-world-health-organization-1.3288355
“Sweets, sugary snacks linked to colorectal cancer” http://www.cbsnews.com/news/sweets-sugary-snacks-linked-to-colorectal-cancer/
“Eating Nuts Linked to Lower Risk of Colon Cancer” http://www.livescience.com/54448-eating-nuts-may-lower-colon-cancer-risk.html
“Coffee consumption linked to lower risk of colorectal cancer” http://www.ctvnews.ca/health/coffee-consumption-linked-to-lower-risk-of-colorectal-cancer-1.2841834
“Alcohol Linked to Colorectal Cancer Risk” http://www.medscape.com/viewarticle/749886
“Excessive alcohol consumption favours high risk polyp or colorectal cancer occurrence among patients with adenomas: a case control study” http://gut.bmj.com/content/50/1/38.full
“High vitamin D levels linked to lower risk of colon cancer” http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/newssummary/news_22-1-2010-13-46-0
“Anthocyanins in Purple, Blue and Red Foods Fight Colon Cancer” http://reliawire.com/anthocyanins-purple-blue-red-foods-fight-colon-cancer/
“Prunes reduce colon cancer risk by benefiting healthy gut bacteria” http://www.belmarrahealth.com/prunes-reduce-colon-cancer-risk-by-benefiting-healthy-gut-bacteria/
“G‐protein coupled receptor 55 (GPR55), a lysophospholipid receptor, has been shown to play an important role in carcinogenesis. GPR55 is involved in the migratory behaviour of colon carcinoma cells and may serve as a pharmacological target for the prevention of metastasis.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4688947/
“The putative cannabinoid receptor GPR55 promotes cancer cell proliferation.” http://www.ncbi.nlm.nih.gov/pubmed/21057532
 “L-α-lysophosphatidylinositol meets GPR55: a deadly relationship. Evidence points to a role of L-α-lysophosphatidylinositol (LPI) in cancer.” http://www.ncbi.nlm.nih.gov/pubmed/21367464
“Modulation of l-α-Lysophosphatidylinositol/GPR55 Mitogen-activated Protein Kinase (MAPK) Signaling by Cannabinoids*Here, we report that the little investigated cannabis constituents CBDV, CBGA, and CBGV are potent inhibitors of LPI-induced GPR55 signaling. The phytocannabinoids Δ9-tetrahydrocannabivarin, cannabidivarin, and cannabigerovarin are also potent inhibitors of LPI. Our findings also suggest that GPR55 may be a new pharmacological target for the following C. sativa constituents: Δ9-THCV, CBDV, CBGA, and CBGV. These Cannabis sativa constituents may represent novel therapeutics targeting GPR55.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249141/
 “Cannabinoids and cancer: potential for colorectal cancer therapy.” https://www.ncbi.nlm.nih.gov/pubmed/16042581
 “The endogenous cannabinoid system protects against colonic inflammation”  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC385396/
 “Cannabinoids in intestinal inflammation and cancer. In vivo, cannabinoids – via direct or indirect activation of CB(1) and/or CB(2) receptors – exert protective effects in well-established models of intestinal inflammation and colon cancer. Pharmacological elevation of endocannabinoid levels may be a promising strategy to counteract intestinal inflammation and colon cancer.” http://www.ncbi.nlm.nih.gov/pubmed/19442536
 “Cannabinoids have become a novel therapeutic approach against colon cancer with protective and anti-tumoral effects on colorectal carcinoma cell lines and in animal models of colon cancer” http://impactjournals.com/oncoscience/index.php?pii=119 
 “Possible endocannabinoid control of colorectal cancer growth. Inhibitors of endocannabinoid inactivation may prove useful anticancer agents.” https://www.ncbi.nlm.nih.gov/pubmed/12949714
“Increased endocannabinoid levels reduce the development of precancerous lesions in the mouse colon. Cannabinoids have been licensed for clinical use as palliative treatment of chemotherapy, but increasing evidence shows antitumor actions of cannabinoid agonists on several tumor cells in vitro and in animal models” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755791/

“Loss of cannabinoid receptor 1 accelerates intestinal tumor growth”  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2561258/

“Turned-off Cannabinoid Receptor Turns On Colorectal Tumor Growth” https://www.sciencedaily.com/releases/2008/08/080801074056.htm

“Turning CB1 back on and then treating with a cannabinoid agonist could provide a new approach to colorectal cancer treatment or prevention. Cannabinoids are a group of ligands that serve a variety of cell-signaling roles. Some are produced by the body internally (endocannabinoids). External cannabinoids include manmade versions and those present in plants, most famously the active ingredient in marijuana (THC).” http://www.news-medical.net/news/2008/08/03/40485.aspx

“Cannabinoid Receptor Activation Induces Apoptosis through Tumor Necrosis Factor α–Mediated Ceramide De novo Synthesis in Colon Cancer Cells. The present study shows that either CB1 or CB2 receptor activation induces apoptosis through ceramide de novo synthesis in colon cancer cells. ” http://clincancerres.aacrjournals.org/content/14/23/7691.long

“The cannabinoid delta(9)-tetrahydrocannabinol inhibits RAS-MAPK and PI3K-AKT survival signalling and induces BAD-mediated apoptosis in colorectal cancer cells. Here, we report that CB1 and CB2 cannabinoid receptors are expressed in human colorectal adenoma and carcinoma cells, and show for the first time that THC induces apoptosis in colorectal cancer cells. The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy.” http://www.ncbi.nlm.nih.gov/pubmed/17583570

“Programmed Cell Death (Apoptosis)” http://www.ncbi.nlm.nih.gov/books/NBK26873/

“Cannabis-Linked Cell Receptor Might Help Prevent Colon Cancer” http://www.medicinenet.com/script/main/art.asp?articlekey=91511

“Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer. Cannabidiol, a safe and non-psychotropic ingredient of Cannabis sativa, exerts pharmacological actions (antioxidant and intestinal antinflammatory) and mechanisms (inhibition of endocannabinoid enzymatic degradation) potentially beneficial for colon carcinogenesis. It is concluded that cannabidiol exerts chemopreventive effect in vivo and reduces cell proliferation through multiple mechanisms.” https://www.ncbi.nlm.nih.gov/pubmed/22231745

“CBD-Rich Marijuana Fights Colon Cancer, New Study Finds” http://blog.sfgate.com/smellthetruth/2014/01/06/cbd-rich-marijuana-fights-colon-cancer-new-study-finds/

“Inhibition of colon carcinogenesis by a standardized Cannabis sativa extract with high content of cannabidiol. Cannabis-based medicines are useful adjunctive treatments in cancer patients.” http://www.ncbi.nlm.nih.gov/pubmed/24373545

“Cannabigerol (CBG) is a safe non-psychotropic Cannabis-derived cannabinoid. CBG hampers colon cancer progression in vivo and selectively inhibits the growth of colorectal cancer cells. CBG should be considered translationally in colorectal cancer prevention and cure.” http://www.ncbi.nlm.nih.gov/pubmed/25269802

“According to researchers at the University of Texas in Houston chemicals in marijuana could be a potential cure in the treatment of colon cancer.” http://www.digitaljournal.com/article/258161

“Cannabis compound clue to colon cancer”  https://www.newscientist.com/article/mg19926685.000-cannabis-compound-clue-to-colon-cancer/

“Marijuana takes on colon cancer” https://www.newscientist.com/article/dn14451-marijuana-takes-on-colon-cancer/

“Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation. In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation. As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.” http://www.cancer.gov/about-cancer/treatment/cam/hp/cannabis-pdq#section/_7

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Dietary ω-3 Polyunsaturated Fatty Acids Inhibit Tumor Growth in Transgenic ApcMin/+ Mice, Correlating with CB1 Receptor Up-Regulation.

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“Mediterranean diet components, such as olive oil and ω-3 polyunsaturated fatty acids (ω-3 PUFAs), can arrest cell growth and promote cell apoptosis.

Recently, olive oil has been demonstrated to modulate type-1 cannabinoid (CB1) receptor gene expression in both human colon cancer cells and rat colon. The aim of this study was to investigate a possible link between olive oil and ω-3 PUFAs effects and CB1 receptor expression in both intestinal and adipose tissue of ApcMin/+ mice.

To confirm the role for the CB1 receptor as a negative modulator of cell proliferation in human colon cancer, CB1 receptor gene expression was also detected in tumor tissue and in surrounding normal mucosa of patients with colorectal cancer (CRC).

Dietary ω-3 PUFAs significantly inhibited intestinal polyp growth in mice, correlating with CB1 receptor gene and protein expression induction. CB1 receptor gene up-regulation was also detected in adipose tissue, suggesting a close communication between cancer cells and the surrounding environment. Tissue CB1 receptor induction was associated with a concurrent inactivation of the Wnt/β-catenin pathway.

Moreover, there was a significant reduction in CB1 receptor gene expression levels in cancer tissue compared to normal surrounding mucosa of patients with CRC, confirming that in cancer the “protective” action of the CB1 receptor is lost.”


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Bladder cancer cell growth and motility implicate cannabinoid 2 receptor-mediated modifications of sphingolipids metabolism.

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“The inhibitory effects demonstrated by activation of cannabinoid receptors (CB) on cancer proliferation and migration may also play critical roles in controlling bladder cancer (BC).

CB expression on human normal and BC specimens was tested by immunohistochemistry.

Human BC cells RT4 and RT112 were challenged with CB agonists and assessed for proliferation, apoptosis, and motility. Cellular sphingolipids (SL) constitution and metabolism were evaluated after metabolic labelling.

CB1-2 were detected in BC specimens, but only CB2 was more expressed in the tumour.

Both cell lines expressed similar CB2. Exposure to CB2 agonists inhibited BC growth, down-modulated Akt, induced caspase 3-activation and modified SL metabolism.

Baseline SL analysis in cell lines showed differences linked to unique migratory behaviours and cytoskeletal re-arrangements.

CB2 activation changed the SL composition of more aggressive RT112 cells by reducing (p < 0.01) Gb3 ganglioside (-50 ± 3%) and sphingosine 1-phosphate (S1P, -40 ± 4%), which ended up to reduction in cell motility (-46 ± 5%) with inhibition of p-SRC.

CB2-selective antagonists, gene silencing and an inhibitor of SL biosynthesis partially prevented CB2 agonist-induced effects on cell viability and motility.

CB2 activation led to ceramide-mediated BC cell apoptosis independently of SL constitutive composition, which instead was modulated by CB2 agonists to reduce cell motility.”


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Cannabinoids – a new weapon against cancer?

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“Cannabis has been cultivated by man since Neolithic times. It was used, among others for fiber and rope production, recreational purposes and as an excellent therapeutic agent.

The isolation and characterization of the structure of one of the main active ingredients of cannabis – Δ9 – tetrahydrocannabinol as well the discovery of its cannabinoid binding receptors CB1 and CB2, has been a milestone in the study of the possibilities of the uses of Cannabis sativa and related products in modern medicine.

Many scientific studies indicate the potential use of cannabinoids in the fight against cancer.

Experiments carried out on cell lines in vitro and on animal models in vivo have shown that phytocannabinoids, endocannabinoids, synthetic cannabinoids and their analogues can lead to inhibition of the growth of many tumor types, exerting cytostatic and cytotoxic neoplastic effect on cells thereby negatively influencing neo-angiogenesis and the ability of cells to metastasize.

The main molecular mechanism leading to inhibition of proliferation of cancer cells by cannabinoids is apoptosis. Studies have shown, however, that the process of apoptosis in cells, treated with recannabinoids, is a consequence of induction of endoplasmic reticulum stress and autophagy. On the other hand, in the cellular context and dosage dependence, cannabinoids may enhance the proliferation of tumor cells by suppressing the immune system or by activating mitogenic factors.

Leading from this there is a an obvious need to further explore cannabinoid associated molecular pathways making it possible to develop safe therapeutic drug agents for patients in the future.”

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