GPR55-Mediated Effects in Colon Cancer Cell Lines

Hasenoehrl, Carina; Feuersinger, David; Kienzl, Melanie; Schicho, Rudolf

doi:10.1159/000496356

Cited by 6 publications

(5 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In all cell lines, except MCF-10A and U-87MG, DHA-DA cytotoxicity was at least partially blocked by both of the two GPR55 antagonists used, indicating that GPR55 is a cell line independent target for cell death induction by this compound ( Figure 5 ). These data agree with the literature data on the GPR55 receptor expression in these cell lines [ 4 , 37 , 38 , 39 , 40 , 41 ].…”

Section: Discussionsupporting

confidence: 93%

GPR55 Receptor Activation by the N-Acyl Dopamine Family Lipids Induces Apoptosis in Cancer Cells via the Nitric Oxide Synthase (nNOS) Over-Stimulation

Akimov

Gamisonia

Dudina

et al. 2021

IJMS

View full text Add to dashboard Cite

GPR55 is a GPCR of the non-CB1/CB2 cannabinoid receptor family, which is activated by lysophosphatidylinositol (LPI) and stimulates the proliferation of cancer cells. Anandamide, a bioactive lipid endocannabinoid, acts as a biased agonist of GPR55 and induces cancer cell death, but is unstable and psychoactive. We hypothesized that other endocannabinoids and structurally similar compounds, which are more hydrolytically stable, could also induce cancer cell death via GPR55 activation. We chemically synthesized and tested a set of fatty acid amides and esters for cell death induction via GPR55 activation. The most active compounds appeared to be N-acyl dopamines, especially N-docosahexaenoyl dopamine (DHA-DA). Using a panel of cancer cell lines and a set of receptor and intracellular signal transduction machinery inhibitors together with cell viability, Ca2+, NO, ROS (reactive oxygen species) and gene expression measurement, we showed for the first time that for these compounds, the mechanism of cell death induction differed from that published for anandamide and included neuronal nitric oxide synthase (nNOS) overstimulation with concomitant oxidative stress induction. The combination of DHA-DA with LPI, which normally stimulates cancer proliferation and is increased in cancer setting, had an increased cytotoxicity for the cancer cells indicating a therapeutic potential.

show abstract

Section: Discussionsupporting

confidence: 93%

GPR55 Receptor Activation by the N-Acyl Dopamine Family Lipids Induces Apoptosis in Cancer Cells via the Nitric Oxide Synthase (nNOS) Over-Stimulation

Akimov

Gamisonia

Dudina

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…As in many other cancer cell lines and tissues, AEA as well as the expression of CB1 was found elevated in CRC [78]. AEA demonstrates an apoptosis-promoting effect per se; this may be interpreted as a selfdefense mechanism.…”

Section: Colorectal Cancermentioning

confidence: 51%

Treatment of malignant diseases with phytocannabinoids: promising observations in animal models and patients

Nahler

2023

Exploration of Medicine

View full text Add to dashboard Cite

Amazingly, almost 50 years after the first demonstration of anticancer effects of cannabinoids in vitro and in vivo, well-designed clinical trials that definitively prove tumour-inhibiting effects in man are still missing. Whereas a large number of preclinical studies exist that describe tumour-inhibiting effects of cannabinoids, alone or in combination, but also in the form of medical cannabis or natural extracts in vitro, the number of in vivo studies is still limited. Even more limited are well-documented experiences in man. Most animal studies and experience with cannabinoids in man concern brain tumours. This review summarises the effects of phytocannabinoids in brain, breast, colorectal, head and neck, haematological, liver, lung, pancreatic, ovarian, prostate, and skin cancers in animal models and, if available, in patients. The large majority of animal studies demonstrate tumour-inhibiting effects of cannabinoids, thus confirming in vitro data. Experiences in cancer patients are almost exclusively limited to individual case reports and case series without a control group. Many questions are currently unanswered such as the role of pure cannabinoids compared to combinations, cannabinoids as the eventual sole cancer therapy, optimal dosages, or duration of treatment. Pure cannabidiol (CBD) seems to be superior to pure delta-9-tetrahydrocannabinol (THC) in experimental settings. The role of medical cannabis or extracts is less clear as they vary in their phytochemical composition. In conclusion, cannabis/cannabinoids may slow the progression of tumours. However, the hope that cannabinoids could eventually cure cancer as often spread in social media, is, at present, wishful thinking. Above all, well-designed clinical trials paired with long-term follow-up of cancer patients are needed.

show abstract

“…GPR55 is part of the endocannabinoid system and its biological function is still under investigation. GPR55 is overexpressed in colon cancerous cells, and may influence ERK1/2 phosphorylation and cell proliferation [ 10 , 11 ]. Carina et al reported that GPR55 is an oncogene in colon cancer, which could contribute to the migration and metastasis of colon cancer cells [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

A comprehensive survival and prognosis analysis of GPR55 expression in hepatocellular carcinoma

Wang,

Xia,

Qiu

et al. 2023

Aging

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is the most common subtype, accounting for about 90% of all primary liver cancers. The liver is rich in a large number of immune cells, thus forming a special immune microenvironment, which plays a key role in the occurrence and development of hepatocellular carcinoma. Nowadays, tumor immunotherapy has become one of the most promising cancer treatment methods. Immune checkpoint inhibitors (ICIs) combined with VEGF inhibitors are listed as first-line treatment options for advanced HCC. Therefore, the search for a potential biomarker to predict the response to immunotherapy in HCC patients is urgently needed. The G protein-coupled receptor 55 ( GPR55 ), a lysophosphatidylinositol (LPI) receptor, has recently emerged as a potential new target for anti-tumor therapy. Previous studies have found that GPR55 is highly expressed in breast cancer, pancreatic cancer, skin cancer and cholangiocarcinoma, and is involved in tumor proliferation and migration. However, the role and mechanism of GPR55 in HCC has not been elucidated. Therefore, this article discusses the clinical significance of GPR55 in HCC and its correlation with the immune response of HCC patients, so as to provide theoretical basis for improving the prognosis of HCC.

show abstract

GPR55-Mediated Effects in Colon Cancer Cell Lines

Cited by 6 publications

References 21 publications

GPR55 Receptor Activation by the N-Acyl Dopamine Family Lipids Induces Apoptosis in Cancer Cells via the Nitric Oxide Synthase (nNOS) Over-Stimulation

GPR55 Receptor Activation by the N-Acyl Dopamine Family Lipids Induces Apoptosis in Cancer Cells via the Nitric Oxide Synthase (nNOS) Over-Stimulation

Treatment of malignant diseases with phytocannabinoids: promising observations in animal models and patients

A comprehensive survival and prognosis analysis of GPR55 expression in hepatocellular carcinoma

Contact Info

Product

Resources

About