ArticlePharmacological research2016
Selective GPR55 antagonism reduces chemoresistance in cancer cells.
Article in Pharmacological research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Astrocytic GPR55 receptors promote glycolysis.Journal of cannabis research · 2026Article
- GPR55 and PINK1 as emerging therapeutic targets in Glioma: insights into their modulation by phytochemicals and plant extracts.Frontiers in pharmacology · 2026Review
- Evaluating the Antitumor Potential of Cannabichromene, Cannabigerol, and Related Compounds fromInternational journal of molecular sciences · 2025Article
- Modulation of neuroinflammation and oxidative stress by targeting GPR55 - new approaches in the treatment of psychiatric disorders.Molecular psychiatry · 2024Review
- GPR55 in the tumor microenvironment of pancreatic cancer controls tumorigenesis.Frontiers in immunology · 2024Article
- Review
- Deprogramming metabolism in pancreatic cancer with a bi-functional GPR55 inhibitor and biased βScientific reports · 2022Article
- Targeting the Endocannabinoidome in Pancreatic Cancer.Biomolecules · 2022Review
- Endocannabinoid System and Tumour Microenvironment: New Intertwined Connections for Anticancer Approaches.Cells · 2021Review
- A short review on cross-link between pyruvate kinase (PKM2) and Glioblastoma Multiforme.Metabolic brain disease · 2021Review
- Nanomedicine to Overcome Multidrug Resistance Mechanisms in Colon and Pancreatic Cancer: Recent Progress.Cancers · 2021Review
- The Glycolytic Pathway as a Target for Novel Onco-Immunology Therapies in Pancreatic Cancer.Molecules (Basel, Switzerland) · 2021Review
- Targeting hypoxic tumor microenvironment in pancreatic cancer.Journal of hematology & oncology · 2021Review
- GPR55 Receptor Activation by theInternational journal of molecular sciences · 2021Article
- ERK is a Pivotal Player of Chemo-Immune-Resistance in Cancer.International journal of molecular sciences · 2019Review
- On the influence of cannabinoids on cell morphology and motility of glioblastoma cells.PloS one · 2019Article
- GPR55 receptor antagonist decreases glycolytic activity in PANC-1 pancreatic cancer cell line and tumor xenografts.International journal of cancer · 2017Article
- Concurrent activation of βCellular signalling · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
G protein-coupled receptor 55 (GPR55) possesses pro-oncogenic activity and its function can be competitively inhibited with (R,R')-4'-methoxy-1-naphthylfenoterol (MNF) through poorly defined signaling pathways. Here, the anti-tumorigenic effect of MNF was investigated in the human pancreatic cancer cell line, PANC-1, by focusing on the expression of known cancer biomarkers and the expression and function of multidrug resistance (MDR) exporters such as P-glycoprotein (Pgp) and breast cancer resistance protein (BCRP). Incubation of PANC1 cells with MNF (1μM) for 24h significantly decreased EGF receptor, pyruvate kinase M2 (PKM2), and β-catenin protein levels and was accompanied by significant reduction in nuclear accumulation of HIF-1α and the phospho-active forms of PKM2 and β-catenin. Inhibition of GPR55 with either MNF or the GPR55 antagonist CID 16020046 lowered the amount of MDR proteins in total cellular extracts while diminishing the nuclear expression of Pgp and BCRP. There was significant nuclear accumulation of doxorubicin in PANC-1 cells treated with MNF and the pre-incubation with MNF increased the cytotoxicity of doxorubicin and gemcitabine in these cells. Potentiation of doxorubicin cytotoxicity by MNF was also observed in MDA-MB-231 breast cancer cells and U87MG glioblastoma cells, which express high levels of GPR55. The data suggest that inhibition of GPR55 activity produces antitumor effects via attenuation of the MEK/ERK and PI3K-AKT pathways leading to a reduction in the expression and function of MDR proteins.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.