ArticlePloS one2017
The G Protein-Coupled Receptor RAI3 Is an Independent Prognostic Factor for Pancreatic Cancer Survival and Regulates Proliferation via STAT3 Phosphorylation.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Prognostic and clinicopathological significance of GPRC5A in various cancers: A systematic review and meta-analysis.PloS one · 2021Pooled it
- The multifaceted roles of the transcriptional coactivator TAZ in extravillous trophoblast development of the human placenta.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Upregulated GPRC5A disrupting the Hippo pathway promotes the proliferation and migration of pancreatic cancer cells via the cAMP-CREB axis.Discover oncology · 2023Article
- Identification of MYEOV-Associated Gene Network as a Potential Therapeutic Target in Pancreatic Cancer.Cancers · 2022Article
- PRMT3 interacts with ALDH1A1 and regulates gene-expression by inhibiting retinoic acid signaling.Communications biology · 2021Article
- GPRC5A: An emerging prognostic biomarker for predicting malignancy of Pancreatic Cancer based on bioinformatics analysis.Journal of Cancer · 2021Article
- Targeting of promising transmembrane proteins for diagnosis and treatment of pancreatic ductal adenocarcinoma.Theranostics · 2021Review
- GPCRs in pancreatic adenocarcinoma: Contributors to tumour biology and novel therapeutic targets.British journal of pharmacology · 2020Review
- Article
- CRISPR/Cas: From Tumor Gene Editing to T Cell-Based Immunotherapy of Cancer.Frontiers in immunology · 2020Review
- LNRRIL6, a novel long noncoding RNA, protects colorectal cancer cells by activating the IL-6-STAT3 pathway.Molecular oncology · 2019Article
- RAI3 is overexpressed in gastric adenocarcinoma but unrelated to prognosis.International journal of clinical and experimental pathology · 2019Article
- Article
- The Effect of GPRC5a on the Proliferation, Migration Ability, Chemotherapy Resistance, and Phosphorylation of GSK-3β in Pancreatic Cancer.International journal of molecular sciences · 2018Article
- Identification of Prognostic Biomarkers by Combined mRNA and miRNA Expression Microarray Analysis in Pancreatic Cancer.Translational oncology · 2018Article
- G Protein-Coupled Receptors as Targets for Approved Drugs: How Many Targets and How Many Drugs?Molecular pharmacology · 2018Review
- GPRC5A: An Emerging Biomarker in Human Cancer.BioMed research international · 2018Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic Ductal Adenocarcinoma (PDAC) is one of the deadliest tumors worldwide. Understanding the function of gene expression alterations is a prerequisite for developing new strategies in diagnostic and therapy. GPRC5A (RAI3), coding for a seven transmembrane G protein-coupled receptor is known to be overexpressed in pancreatic cancer and might be an interesting candidate for therapeutic intervention. Expression levels of RAI3 were compared using a tissue microarray of 435 resected patients with pancreatic cancer as well as 209 samples from chronic pancreatitis (CP), intra-ductal papillary mucinous neoplasm (IPMN) and normal pancreatic tissue. To elucidate the function of RAI3 overexpression, siRNA based knock-down was used and transfected cells were analyzed using proliferation and migration assays. Pancreatic cancer patients showed a statistically significant overexpression of RAI3 in comparison to normal and chronic pancreatitis tissue. Especially the loss of apical RAI3 expression represents an independent prognostic parameter for overall survival of patients with pancreatic cancer. Suppression of GPRC5a results in decreased cell growth, proliferation and migration in pancreatic cancer cell lines via a STAT3 modulated pathway, independent from ERK activation.
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