Cannabinoids Inhibit Cellular Respiration of Human Oral Cancer Cells

Whyte, Donna A.; Al‐Hammadi, Suleiman; Balhaj, Ghazala; Brown, Oliver M.; Penefsky, Harvey S.; Souid, Abdul Kader

doi:10.1159/000312686

Cited by 45 publications

(29 citation statements)

References 31 publications

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“…Engagement of these receptors on immune cells has been shown to suppress pro-inflammatory cytokine production and enhance anti-inflammatory cytokine production (38, 39) leading to reduced host immune responses to infectious agents as well as suppression of anti-tumor immunity (40–42). Conversely, Δ (9) -THC has also been shown in epithelial cell lines to have distinct antitumor effects through arrest of uncontrolled cell growth, enhancement of apoptosis, and downregulation of angiogenesis and cellular migration (43–45). As a result, this cannabinoid has been investigated as a potential therapeutic agent in the treatment of glioma, breast and prostate cancers (46, 47).…”

Section: Discussionmentioning

confidence: 99%

Association of Marijuana Smoking with Oropharyngeal and Oral Tongue Cancers: Pooled Analysis from the INHANCE Consortium

Marks

Chaturvedi

Kelsey

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background The incidence of oropharyngeal and oral tongue cancers have increased over the last twenty years which parallels increased use of marijuana among individuals born after 1950. Methods Pooled analysis of individual-level data from nine case-control studies from the U.S. and Latin America in the INHANCE consortium. Self-reported information on marijuana smoking, demographic, and behavioral factors was obtained from 1,921 oropharyngeal cases, 356 oral tongue cases, and 7,639 controls. Results Compared with never marijuana smokers, ever marijuana smokers had an elevated risk of oropharyngeal (adjusted odds ratio [aOR]: 1.24; 95% confidence interval [CI]: 1.06, 1.47) and a reduced risk of oral tongue cancer (aOR: 0.47; 95% CI: 0.29, 0.75). The risk of oropharyngeal cancer remained elevated among never tobacco and alcohol users. The risk of oral tongue cancer decreased with increasing frequency (ptrend=0.005), duration (ptrend=0.002), and joint-years of marijuana use (ptrend=0.004), and was reduced among never users tobacco and alcohol users. Sensitivity analysis adjusting for potential confounding by HPV exposure attenuated the association of marijuana use with oropharyngeal cancer (aOR: 0.99; 95% CI: 0.71, 1.25), but had no effect on the oral tongue cancer association. Conclusions These results suggest that the association of marijuana use with Head and Neck Carcinoma may differ by tumor site. Impact The associations of marijuana use with oropharyngeal and oral tongue cancer are consistent with both possible pro- and anti-carcinogenic effects of cannabinoids. Additional work is needed to rule out various sources of bias, including residual confounding by HPV infection and misclassification of marijuana exposure.

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Section: Discussionmentioning

confidence: 99%

Association of Marijuana Smoking with Oropharyngeal and Oral Tongue Cancers: Pooled Analysis from the INHANCE Consortium

Marks

Chaturvedi

Kelsey

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Cannabidiol (CBD)-induced endoplasmic reticulum stress mediated cell death of MDA-MB231 breast cancer cells, with the coexistence of autophagy and apoptosis [63]. Recently one published report shows that Δ 9 -THC and Δ 8 -THC inhibited mitochondrial oxygen consumption rate via receptor independent manner in oral cancer cells [152]. In primary lymphocytes, treatment with CBD induced caspase 8 induced apoptosis which was mediated by oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Cannabinoids as therapeutic agents in cancer: current status and future implications

2014

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The pharmacological importance of cannabinoids has been in study for several years. Cannabinoids comprise of (a) the active compounds of the Cannabis sativa plant, (b) endogenous as well as (c) synthetic cannabinoids. Though cannabinoids are clinically used for anti-palliative effects, recent studies open a promising possibility as anti-cancer agents. They have been shown to possess anti-proliferative and anti-angiogenic effects in vitro as well as in vivo in different cancer models. Cannabinoids regulate key cell signaling pathways that are involved in cell survival, invasion, angiogenesis, metastasis, etc. There is more focus on CB1 and CB2, the two cannabinoid receptors which are activated by most of the cannabinoids. In this review article, we will focus on a broad range of cannabinoids, their receptor dependent and receptor independent functional roles against various cancer types with respect to growth, metastasis, energy metabolism, immune environment, stemness and future perspectives in exploring new possible therapeutic opportunities.

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“…Cannabinoid receptor agonists are reported to inhibit cellular respiration in human sperm and cancer cells [40, 41]. They also reduce UCP-1 and adiponectin expression in brown and white adipocytes, respectively, and increase visfatin expression in white adipocytes, to collectively inhibit thermogenesis and promote a positive energy balance [42].…”

Section: Discussionmentioning

confidence: 99%

Testosterone Rapidly Augments Retrograde Endocannabinoid Signaling in Proopiomelanocortin Neurons to Suppress Glutamatergic Input from Steroidogenic Factor 1 Neurons via Upregulation of Diacylglycerol Lipase-α

Conde

Fabelo²,

Krause³

et al. 2016

Neuroendocrinology

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Testosterone exerts profound effects on reproduction and energy homeostasis. Like other orexigenic hormones, it increases endocannabinoid tone within the hypothalamic feeding circuitry. Therefore, we tested the hypothesis that testosterone upregulates the expression of diacylglycerol lipase (DAGL)α in the hypothalamic arcuate nucleus (ARC) to increase energy intake via enhanced endocannabinoid-mediated retrograde inhibition of anorexigenic proopiomelanocortin (POMC) neurons. Energy intake, meal patterns, and energy expenditure were evaluated in orchidectomized, male guinea pigs treated subcutaneously with testosterone propionate (TP; 400 μg) or its sesame oil vehicle (0.1 mL). TP rapidly increased energy intake, meal size, O₂ consumption, CO₂ production, and metabolic heat production, all of which were antagonized by prior administration of the DAGL inhibitor orlistat (3 μg) into the third ventricle. These orlistat-sensitive, TP-induced increases in energy intake and expenditure were temporally associated with a significant elevation in ARC DAGLα expression. Electrophysiological recordings in hypothalamic slices revealed that TP potentiated depolarization-induced suppression of excitatory glutamatergic input onto identified ARC POMC neurons, which was also abolished by orlistat (3 μM), the CB₁ receptor antagonist AM251 (1 μM), and the AMP-activated protein kinase inhibitor compound C (30 μM) and simulated by transient bath application of the dihydrotestosterone mimetic Cl-4AS-1 (100 nM) and testosterone-conjugated bovine serum albumin (100 nM). Thus, testosterone boosts DAGLα expression to augment retrograde, presynaptic inhibition of glutamate release onto ARC POMC neurons that, in turn, increases energy intake and expenditure. These studies advance our understanding of how androgens work within the hypothalamic feeding circuitry to affect changes in energy balance.

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Cannabinoids Inhibit Cellular Respiration of Human Oral Cancer Cells

Cited by 45 publications

References 31 publications

Association of Marijuana Smoking with Oropharyngeal and Oral Tongue Cancers: Pooled Analysis from the INHANCE Consortium

Association of Marijuana Smoking with Oropharyngeal and Oral Tongue Cancers: Pooled Analysis from the INHANCE Consortium

Cannabinoids as therapeutic agents in cancer: current status and future implications

Testosterone Rapidly Augments Retrograde Endocannabinoid Signaling in Proopiomelanocortin Neurons to Suppress Glutamatergic Input from Steroidogenic Factor 1 Neurons via Upregulation of Diacylglycerol Lipase-α

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