ArticleCancer science2004
Cloning of a G-protein-coupled receptor that shows an activity to transform NIH3T3 cells and is expressed in gastric cancer cells.
Article in Cancer science, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 88 citations in OpenAlex.
- An epithelial GPR35 isoform supports tumor-associated transcriptional and metabolic phenotypes.FEBS letters · 2026Article
- Dietary anthocyanidin pelargonidin activates G protein-coupled receptor 35.The FEBS journal · 2026Article
- GPR35-mediated metabolic reprogramming promotes tumorigenesis in digestive cancers.Frontiers in immunology · 2025Review
- From orphan to oncogene: The role of GPR35 in cancer and immune modulation.Cytokine & growth factor reviews · 2024Review
- Pharmacohistory of Cannabis Use-A New Possibility in Future Drug Development for Gastrointestinal Diseases.International journal of molecular sciences · 2023Review
- The cryptic role of CXCL17/CXCR8 axis in the pathogenesis of cancers: a review of the latest evidence.Journal of cell communication and signaling · 2023Review
- Recent advances in GPR35 pharmacology; 5-HIAA serotonin metabolite becomes a ligand.Archives of pharmacal research · 2023Review
- GPR35 acts a dual role and therapeutic target in inflammation.Frontiers in immunology · 2023Review
- GPR35 antagonist CID-2745687 attenuates anchorage-independent cell growth by inhibiting YAP/TAZ activity in colorectal cancer cells.Frontiers in pharmacology · 2023Article
- Involvement of CXCL17 and GPR35 in Gastric Cancer Initiation and Progression.International journal of molecular sciences · 2022Article
- Review
- Article
- Lipopeptide Pepducins as Therapeutic Agents.Methods in molecular biology (Clifton, N.J.) · 2022Article
- G-protein coupled receptor 35 (GPR35) regulates the colonic epithelial cell response to enterotoxigenic Bacteroides fragilis.Communications biology · 2021Article
- Metabolic Functions of G Protein-Coupled Receptors and β-Arrestin-Mediated Signaling Pathways in the Pathophysiology of Type 2 Diabetes and Obesity.Frontiers in endocrinology · 2021Review
- GPR35 in Intestinal Diseases: From Risk Gene to Function.Frontiers in immunology · 2021Review
- Therapeutic Opportunities and Challenges in Targeting the Orphan G Protein-Coupled Receptor GPR35.ACS pharmacology & translational science · 2020Review
- Antitumor Activity of Abnormal Cannabidiol and Its Analog O-1602 in Taxol-Resistant Preclinical Models of Breast Cancer.Frontiers in pharmacology · 2019Article
- GPR35 promotes glycolysis, proliferation, and oncogenic signaling by engaging with the sodium potassium pump.Science signaling · 2019Article
- Adopting an Orphan: How Could GRP35 Contribute to Angiotensin II-Dependent Hypertension?American journal of hypertension · 2018Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was directed towards the identification of novel factors involved in the transformation process leading to the formation of gastric cancer. A cDNA library from human gastric cancer cells was constructed using a retroviral vector. Functional cloning was performed by screening for transformation activity in transduced NIH3T3 cells. Six cDNA clones were isolated, including one encoding the elongation factor 1alpha subunit, which was already known to play a role in tumorigenesis. One cDNA (clone 56.2), which was repeatedly isolated during the course of screening, encoded a protein identical to a G-protein-coupled receptor protein, GPR35. In addition, another cDNA clone (72.3) was found to be an alternatively spliced product of the GPR35 gene, whereby 31 amino acids were added to the N-terminus of GPR35. Hence, the proteins encoded by clones 56.2 and 72.3 were designated GPR35a and GPR35b, respectively. RT-PCR experiments revealed that GPR35 gene expression is low or absent in surrounding non-cancerous regions, while both mRNAs were present in all of the gastric cancers examined. The level of 72.3-encoded mRNA was consistently significantly higher than that of 56.2 encoded mRNA. An expression pattern similar to that observed in gastric cancers was detected in normal intestinal mucosa. Based on the apparent transformation activities of the two GPR35 clones in NIH3T3 cells, and the marked up-regulation of their expression levels in cancer tissues, it is speculated that these two novel isoforms of GPR35 are involved in the course of gastric cancer formation.
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