Influence of Δ9-tetrahydrocannabinol on cell proliferation and macromolecular biosynthesis in human cells

Mon, Manuel J.; Jansing, Robert L.; Doggett, Stephen L.; Stein, Janet L.

doi:10.1016/0006-2952(78)90553-1

Cited by 36 publications

(15 citation statements)

References 28 publications

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“…The glycoprotein gD has been reported to account for cross-neutralization between HSVl and HSV2 (28). The decreases in virus-specified protein synthesis recorded for the present study are in agreement with reports that A9-THC suppresses macromolecular synthesis in various mammalian culture systems (6,29).…”

Section: Drug Administration and Virus Infectionsupporting

confidence: 94%

Inhibition of Cell-Associated Herpes Simplex Virus Type 2 Glycoproteins by 9-Tetrahydrocannabinol

Mishkin

Cabral

1987

Experimental Biology and Medicine

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This study was conducted to define the effect of micromolar concentrations of A'-tetrahydrocannabinol ( A'-THC) on the biosynthesis and expression of herpes simplex virus type 2 (HSV2)-specified glycoproteins. Dose-related reductions in all species of virus glycoproteins were recorded by one-dimensional SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and autoradiography of [ ''C]glucosamine-labeled infected Vero cells treated with lo-' to lo-' M A'-THC. A drug dose-related depletion of the mature HSV2 major envelope glycoprotein complex ( 1 1 9-kDa average molecular weight), accompanied by accumulation of immature unglycosylated species, was demonstrated by two-dimensional SDS-PAGE in concert with Western immunoblotting or autoradiography. Light and electron microscopy immunoperoxidase staining revealed that A'-THC effected depletion of 119-kDa determinants from the infected cell surface. This depletion occurred concomitantly with accumulation of 1 19-kDa components at the pennucleus. However, the expression of 1 19-kDa glycoproteins on the virion envelope was not affected. These results indicate that A'-THC inhibits the synthesis, maturation, and cellular transport of HSV2specified glycoproteins. Decreased expression of virus glycoproteins on the infected cell surface may affect host immune responsiveness to HSV2.

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Section: Drug Administration and Virus Infectionsupporting

confidence: 94%

Inhibition of Cell-Associated Herpes Simplex Virus Type 2 Glycoproteins by 9-Tetrahydrocannabinol

Mishkin

Cabral

1987

Experimental Biology and Medicine

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“…Central to any discussion of genotoxic mechanisms of cannabis are considerations of the biological mechanisms by which it mediates chromosomal derangements and disruptions. Cannabis and the cannabinoids THC, cannabinol, cannabidiol and cannabinol have been shown to be toxic to oocytes 6 , sperm 24 , 95 , 96 , chromosomes 96 , the bases of DNA 97 and epigenetic regulation both by DNA methylation 4 , 19 , 20 , 22 – 24 , 98 and histone formation 16 , 99 . Cannabidiol and cannabidivarin in low doses have been shown to directly oxidize DNA bases which is a highly oncogenic and mutagenic action 97 .…”

Section: Discussionmentioning

confidence: 99%

“…Cannabidiol and cannabidivarin in low doses have been shown to directly oxidize DNA bases which is a highly oncogenic and mutagenic action 97 . Cannabinoids have long been recognized to reduce the synthesis of major macromolecules of life including DNA, RNA proteins and histones 13 , 18 , 60 , 99 – 104 . Reduction in the linker histone H1 has recently been shown to comprise a major oncogenic mechanism by making genes more accessible for transcription 105 .…”

Section: Discussionmentioning

confidence: 99%

Epidemiological overview of multidimensional chromosomal and genome toxicity of cannabis exposure in congenital anomalies and cancer development

Reece

Hulse

2021

Sci Rep

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Cannabis and cannabinoids are implicated in multiple genotoxic, epigenotoxic and chromosomal-toxic mechanisms and interact with several morphogenic pathways, likely underpinning previous reports of links between cannabis and congenital anomalies and heritable tumours. However the effects of cannabinoid genotoxicity have not been assessed on whole populations and formal consideration of effects as a broadly acting genotoxin remain unexplored. Our study addressed these knowledge gaps in USA datasets. Cancer data from CDC, drug exposure data from National Survey of Drug Use and Health 2003–2017 and congenital anomaly data from National Birth Defects Prevention Network were used. We show that cannabis, THC cannabigerol and cannabichromene exposure fulfill causal criteria towards first Principal Components of both: (A) Down syndrome, Trisomies 18 and 13, Turner syndrome, Deletion 22q11.2, and (B) thyroid, liver, breast and pancreatic cancers and acute myeloid leukaemia, have mostly medium to large effect sizes, are robust to adjustment for ethnicity, other drugs and income in inverse probability-weighted models, show prominent non-linear effects, have 55/56 e-Values > 1.25, and are exacerbated by cannabis liberalization (P = 9.67 × 10–43, 2.66 × 10–15). The results confirm experimental studies showing that cannabinoids are an important cause of community-wide genotoxicity impacting both birth defect and cancer epidemiology at the chromosomal hundred-megabase level.

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“…The influence of cannabinoids on the proliferation of human cervical adenocarcinoma cells and on macromolecular biosynthetic events associated with the proliferative process were reported in the late 1970s when cannabinoids induced growth inhibition of HeLa cells, human cervical cancer cell lines (Blevins et al, 1980;Mon et al, 1978). More recently, an up-regulation of both cannabinoid receptors in human ovarian cancer cells OVCAR-3 and SKOV-3 compared to normal Chinese hamster ovarian (CHO) cells was found.…”

Section: Cannabinoids and Reproductive System Cancermentioning

confidence: 90%

Cannabinoid pharmacology in cancer research: A new hope for cancer patients?

Javid

Phillips

Afshinjavid

et al. 2016

European Journal of Pharmacology

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Cannabinoids have been used for many centuries to ease pain and in the past decade, the endocannabinoid system has been implicated in a number of pathophysiological conditions, such as mood and anxiety disorders, movement disorders such as Parkinson's and Huntington's disease, neuropathic pain, multiple sclerosis, spinal cord injury, atherosclerosis, myocardial infarction, stroke, hypertension, glaucoma, obesity, and osteoporosis. Several studies have demonstrated that cannabinoids also have anti-cancer activity and as cannabinoids are usually well tolerated and do not produce the typical toxic effects of conventional chemotherapies, there is considerable merit in the development of cannabinoids as potential anticancer therapies. Whilst the presence of psychoactive effects of cannabinoids could prevent any progress in this field, recent studies have shown the value of the non-psychoactive components of cannabinoids in activating apoptotic pathways, inducing anti-proliferative and anti-angiogenic effects. The aforementioned effects are suggested to be through pathways such as ERK, Akt, mitogen-activated protein kinase (MAPK) pathways, phosphoinositide 3-kinase (PI3K) pathways and hypoxia inducible factor 1 (HIF1), all of which are important contributors to the hallmarks of cancer. Many important questions still remain unanswered or are poorly addressed thus necessitating further research at basic pre-clinical and clinical levels. In this review, we address these issues with a view to identifying the key challenges that future research needs to address.

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Influence of Δ9-tetrahydrocannabinol on cell proliferation and macromolecular biosynthesis in human cells

Cited by 36 publications

References 28 publications

Inhibition of Cell-Associated Herpes Simplex Virus Type 2 Glycoproteins by 9-Tetrahydrocannabinol

Inhibition of Cell-Associated Herpes Simplex Virus Type 2 Glycoproteins by 9-Tetrahydrocannabinol

Epidemiological overview of multidimensional chromosomal and genome toxicity of cannabis exposure in congenital anomalies and cancer development

Cannabinoid pharmacology in cancer research: A new hope for cancer patients?

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