ArticleMedical cannabis and cannabinoids2019
GPR55-Mediated Effects in Colon Cancer Cell Lines.
Article in Medical cannabis and cannabinoids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- The Interaction of the Endocannabinoid Anandamide and Paracannabinoid Lysophosphatidylinositol during Cell Death Induction in Human Breast Cancer Cells.International journal of molecular sciences · 2024Article
- Exploring orphan GPCRs in neurodegenerative diseases.Frontiers in pharmacology · 2024Review
- GPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis.Frontiers in immunology · 2024Article
- A comprehensive survival and prognosis analysis of GPR55 expression in hepatocellular carcinoma.Aging · 2023Article
- GPR55 Receptor Activation by theInternational journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cannabinoid-responsive G protein-coupled receptor GPR55 and its endogenous ligand L-α-lysophosphatidyl-inositol (LPI) have been reported to play a role in several cancers. A proliferation-enhancing effect of GPR55 has been described for several cancer cell lines and LPI has been found elevated in cancer patients. The aim of this study was to investigate whether GPR55 signaling had an effect on the proliferation of colon cancer cell lines. Using cell viability assays and Western blotting, we show that stable overexpression of the GPR55 receptor led to a growth advantage of SW480 cells per se. Proliferation of native colon cancer cell lines, however, was not affected by pharmacological manipulation of GPR55. Interestingly though, GPR55 signaling was responsive to treatment with both the GPR55 agonist LPI and the antagonist CID16020046 in the overexpressing cancer cell lines. This was evident through significantly increased or decreased levels of phosphorylated ERK1/2, respectively. Taken together, our findings suggest that GPR55 is constitutively activated in overexpressing colon cancer cells affecting ERK1/2 phosphorylation and cell proliferation.
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Registered trials
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