
THC inhibited several processes involved in the growth and spread of endometrial cancer cells. In laboratory experiments, Δ9-THC reduced cancer-cell viability and motility and suppressed epithelial-mesenchymal transition (EMT), a process that helps cancer cells become more invasive and capable of spreading.
The study found that THC also reduced matrix metalloproteinase-9 (MMP-9), an enzyme that helps tumor cells break through surrounding tissue and is strongly associated with invasion and metastasis. By targeting MMP-9 and reversing EMT-related changes, THC interfered with mechanisms that endometrial cancer cells use to migrate and spread.
These findings suggest that THC may have potential to affect not only tumor-cell growth, but also the biological processes that drive invasion and metastasis in endometrial cancer. The study adds to evidence that cannabinoids can influence multiple cancer-related pathways beyond simple cell-killing effects.
“Limited therapeutic interventions are clinically available for treating aggressive endometrial cancer (EC). Therefore, effective therapies are urgently required.
Therefore, the present study investigated the role of ∆9-tetrahydrocannabinol (THC), which is reported to impact proliferative and migratory activities during impairment of cancer progression.
In the present study, cell migration in response to THC was measured using transwell assays. Using western blot analysis, the levels of cannabinoid receptors in EC tissues were detected and pathways leading to the inhibition of cell migration by THC on human EC cells were determined.
Results suggested that cannabinoid receptors were highly expressed in EC tissues. Furthermore, THC inhibited EC cell viability and motility by inhibiting epithelial-mesenchymal transition (EMT) and downregulating matrix metalloproteinase-9 (MMP-9) gene expression in aggressive human EC cells.
The results have the potential to promote the development of novel compounds for the treatment of EC metastasis. The presnet findings suggest that THC may inhibit human EC cell migration through regulating EMT and MMP-9 pathways.”
https://pubmed.ncbi.nlm.nih.gov/29805589
“This current study found that cannabinoid receptors were over expressed in EC tissues and the protein levels were positively correlated with EMT markers. Furthermore, THC has been proven to inhibit EC cell motility and EMT through reducing MMP-9, which makes THC become a novel tumor suppressor in EC.”
https://www.spandidos-publications.com/10.3892/ol.2018.8407
Need this THC study explained? thcXplained.com
“Pain is a serious health problem that is commonly treated with opioids, although the doses of opioids needed to treat pain are often similar to those that decrease respiration. Combining opioids with drugs that relieve pain through non-opioid mechanisms can decrease the doses of opioids needed for analgesia, resulting in an improved therapeutic window, but only if the doses of opioids that decrease respiration are not similarly decreased. Using small doses of opioids to treat pain has the potential to reduce the number of overdoses and deaths.
This study investigated whether the
“Nearly half a century has passed since the demonstration that cannabis and its chief psychoactive component Δ⁸-THC lowers intraocular pressure (IOP).
Elevated IOP remains the chief hallmark and therapeutic target for glaucoma, a condition that places millions at risk of blindness. It is likely that Δ⁸-THC exerts much of its IOP-lowering effects via the activation of CB1 cannabinoid receptors.
However, the initial promise of CB1 as a target for treating glaucoma has not thus far translated into a credible therapeutic strategy. We have recently shown that blocking monoacylglycerol lipase (MAGL), an enzyme that breaks the endocannabinoid 2-arachidonoyl glycerol (2-AG), substantially lowers IOP.
Another strategy is to develop cannabinoid CB1 receptor agonists that are optimized for topical application to the eye. Recently we have reported on a controlled-deactivation approach where the “soft” drug concept of enzymatic deactivation was combined with a “depot effect” that is commonly observed with Δ⁸-THC and other lipophilic cannabinoids.
This approach allowed us to develop novel cannabinoids with a predictable duration of action and is particularly attractive for the design of CB1 activators for ophthalmic use with limited or no psychoactive effects.
We have tested a novel class of compounds using a combination of electrophysiology in autaptic hippocampal neurons, a well-characterized model of endogenous cannabinoid signaling, and measurements of IOP in a mouse model.
We now report that AM7410 is a reasonably potent and efficacious agonist at CB1 in neurons and that it substantially (30%) lowers IOP for as long as 5 h after a single topical treatment. This effect is absent in CB1 knockout mice.
Our results indicate that the direct targeting of CB1 receptors with controlled-deactivation ligands is a viable approach to lower IOP in a murine model and merits further study in other model systems.”
“A complex motor disorder is a combination of various types of abnormal movements that are associated with impaired quality of life (QOL). Current therapeutic options are limited. We studied the efficacy, safety, and tolerability of medical
“Phytocannabinoids, such as Δ9–