ArticleCancer research2009
The G protein-coupled receptor 87 is necessary for p53-dependent cell survival in response to genotoxic stress.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- GPR87 promotes tumor cell invasion and mediates the immunogenomic landscape of lung adenocarcinoma.Communications biology · 2022Pooled it
- Near Infrared Photoimmunotherapy for Lung Cancer: Recent Development and Perspective.ImmunoTargets and therapy · 2026Review
- Idiopathic Pulmonary Fibrosis: Cellular Heterogeneity, Mechanisms, and Therapeutic Implications.MedComm · 2025Review
- Increased reflux secondary bile acids are associated with changes to the microbiome and transcriptome in Barrett's esophagus.Gut microbes · 2025Article
- The path of GPR87: from a P2Y-like receptor to its role in cancer progression.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Molecular Dynamics (MD) Simulation of GPR87-LPA Binding: Therapeutic Implications for Targeted Cancer Treatment.Anti-cancer agents in medicinal chemistry · 2025Article
- Orphan Class A GPCRs Signature Predicts Prognosis and Immune Microenvironment in Gastric Cancer: GPR176 Drives Tumor Progression Through Wnt Signaling and Macrophage Polarization.Mediators of inflammation · 2025Article
- G-protein-coupled receptor 141 mediates breast cancer proliferation and metastasis by regulating oncogenic mediators and the p-mTOR/p53 axis.Oncotarget · 2023Article
- Identification of Key Genes and Pathways in Genotoxic Stress Induced Endothelial Dysfunction: Results of Whole Transcriptome Sequencing.Biomedicines · 2022Article
- Single-cell RNA sequencing identifies G-protein coupled receptor 87 as a basal cell marker expressed in distal honeycomb cysts in idiopathic pulmonary fibrosis.The European respiratory journal · 2022Article
- The landscape of receptor-mediated precision cancer combination therapy via a single-cell perspective.Nature communications · 2022Article
- Article
- Transcriptome Profiling Reveals a Divergent Adaptive Response to Hyper- and Hypo-Salinity in the Yellow Drum,Animals : an open access journal from MDPI · 2021Article
- Pancreatic Adenocarcinoma: Unconventional Approaches for an Unconventional Disease.Cancer research · 2020Review
- Development and validation of a metastasis-related Gene Signature for predicting the Overall Survival in patients with Pancreatic Ductal Adenocarcinoma.Journal of Cancer · 2020Article
- EDNRB isoform 3 confers Temozolomide resistance in A375 melanoma cells by modulating membrane potential, reactive oxygen species and mitochondrial CaCancer management and research · 2019Article
- Article
- Census and evaluation of p53 target genes.Oncogene · 2017Review
- Overexpression of G protein-coupled receptor GPR87 promotes pancreatic cancer aggressiveness and activates NF-κB signaling pathway.Molecular cancer · 2017Article
- Nasal DNA methylation differentiates corticosteroid treatment response in pediatric asthma: A pilot study.PloS one · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
p53 regulates an array of target genes, which mediates p53 tumor suppression by inducing cell cycle arrest, apoptosis, and cell survival. G protein-coupled receptors belong to a superfamily of cell surface molecules and are known to regulate cell proliferation, migration, and survival. Here, we found that G protein-coupled receptor 87 (GPR87) was up-regulated by p53 and by DNA damage in a p53-dependent manner. We also found that p53 directly regulated GPR87 potentially via a p53-responsive element in the GPR87 gene. To investigate the role of GPR87 in the p53 pathway, we generated multiple RKO and MCF7 cell lines in that GPR87 can be inducibly overexpressed or knocked down by a tetracycline-inducible system. We found that overexpression of GPR87 had little effect on cell growth. However, GPR87 knockdown sensitized cancer cells to DNA damage-induced growth suppression via enhanced p53 stabilization and activation. Importantly, the prosurvival activity of GPR87 can be reversed by knockdown of p53. Together, our results suggested that GPR87 is essential for p53-dependent cell survival in response to DNA damage. Thus, due to its expression on the cell surface and its role in cell survival, GPR87 may be explored as a novel therapeutic target for cancer treatment and prevention.
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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.