ArticleOncology reports2018
GPR56 promotes proliferation of colorectal cancer cells and enhances metastasis via epithelial‑mesenchymal transition through PI3K/AKT signaling activation.
Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 57 citations in OpenAlex.
- Platelet-Prostate cancer crosstalk driving disparities and therapeutic vulnerabilities.Discover oncology · 2026Review
- The Role of the TG2-GPR56 Complex in Cutaneous Squamous Cell Carcinoma (CSCC) Aggression and Therapeutic Resistance.International journal of molecular sciences · 2026Review
- GPR56 function as a key repressor in hepatocyte pyroptosis and the pathogenesis of liver fibrosis.Journal of translational medicine · 2025Article
- GPR56/ADGRG1 induces biased Rho-ROCK-MLC and JAK-STAT3 signaling to promote amoeboid-like morphology and IL-6 upregulation in melanoma cells.Cell communication and signaling : CCS · 2025Article
- Article
- Mechanisms of Peptide Agonist Dissociation and Deactivation of Adhesion G-Protein-Coupled Receptors.Biochemistry · 2025Article
- The Use of Biologics for Targeting GPCRs in Metastatic Cancers.Biotech (Basel (Switzerland)) · 2025Review
- GPR56 facilitates hepatocellular carcinoma metastasis by promoting the TGF-β signaling pathway.Cell death & disease · 2024Article
- Loss of cardiomyocyte-specific adhesion G-protein-coupled receptor G1 (ADGRG1/GPR56) promotes pressure overload-induced heart failure.Bioscience reports · 2024Article
- Mechanisms of peptide agonist dissociation and deactivation of adhesion G-protein-coupled receptors.bioRxiv : the preprint server for biology · 2024Article
- Upregulation of EMR1 (ADGRE1) by Tumor-Associated Macrophages Promotes Colon Cancer Progression by Activating the JAK2/STAT1,3 Signaling Pathway in Tumor Cells.International journal of molecular sciences · 2024Article
- Multi-omics identification of GPCR gene features in lung adenocarcinoma based on multiple machine learning combinations.Journal of Cancer · 2024Article
- Increased glycolysis and cellular crosstalk in eosinophilic chronic rhinosinusitis with nasal polyps.Frontiers in immunology · 2024Article
- GPR56, an Adhesion GPCR with Multiple Roles in Human Diseases, Current Status and Future Perspective.Current drug targets · 2024Review
- Biophysics in tumor growth and progression: from single mechano-sensitive molecules to mechanomedicine.Oncogene · 2023Review
- GPR114/ADGRG5 is activated by its tethered peptide agonist because it is a cleaved adhesion GPCR.The Journal of biological chemistry · 2023Article
- Current Landscape of Genome-Wide Association Studies in Acute Myeloid Leukemia: A Review.Cancers · 2023Review
- Hexahydroquinoline Derivatives Are Selective Agonists for the Adhesion G Protein-Coupled Receptor ADGRG1/GPR56.Molecular pharmacology · 2023Article
- Signaling pathways in cancer metabolism: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- GPR176 Promotes Cancer Progression by Interacting with G Protein GNAS to Restrain Cell Mitophagy in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G protein‑coupled receptor 56 (GPR56), a member of the orphan GPCR family, has been reported to be an oncogene in various malignancies. However, little is known regarding the detailed molecular mechanism of GPR56 in colorectal cancer (CRC). The present study aimed to detect the expression level and biological function of GPR56 in CRC. We examined the expression of GPR56 in CRC tissues and cell lines by quantitative real time (qRT)‑PCR, immunohistochemistry, and western blot analysis. The prognostic significance of GPR56 in CRC patients was evaluated by Kaplan‑Meier survival analysis. The influence of GPR56 on tumor cell proliferation (via Cell Counting Kit‑8, and a tumor formation assay in mice), apoptosis (flow cytometry), cell cycle distribution (flow cytometry) and migration (Transwell assay) was explored. We also investigated the underlying mechanism of GPR56 by western blot analysis. We found GPR56 expression was significantly upregulated in CRC tissues and cell lines compared to corresponding normal controls. Higher GPR56 expression in patients predicted poorer prognosis. Depletion of GPR56 markedly suppressed cell proliferation, migration, and invasion. GPR56 overexpression promoted CRC cell metastasis by expediting epithelial‑mesenchymal transition by activating PI3K/AKT signaling. In conclusion, GPR56 played an important role in CRC progression and may represent a new therapeutic target to reduce CRC metastasis.
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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.