ArticlePloS one2010
Comparative functional genomics analysis of NNK tobacco-carcinogen induced lung adenocarcinoma development in Gprc5a-knockout mice.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Prognostic and clinicopathological significance of GPRC5A in various cancers: A systematic review and meta-analysis.PloS one · 2021Pooled it
- G protein-coupled receptors as novel therapeutic targets in non-small-cell lung cancer.Medical review (2021) · 2025Review
- Mutation of SMARCA4 Induces Cancer Cell-Intrinsic Defects in the Enhancer Landscape and Resistance to Immunotherapy.Cancer research · 2025Article
- Selective inhibition of canonical STAT3 signaling suppresses K-ras mutant lung tumorigenesis and reinvigorates anti-tumor immunity.Frontiers in immunology · 2025Article
- Inflammation Mediated by Gut Microbiome Alterations Promotes Lung Cancer Development and an Immunosuppressed Tumor Microenvironment.Cancer immunology research · 2024Article
- Article
- Syngeneic tobacco carcinogen-induced mouse lung adenocarcinoma model exhibits PD-L1 expression and high tumor mutational burden.JCI insight · 2021Article
- Augmented Lipocalin-2 Is Associated with Chronic Obstructive Pulmonary Disease and Counteracts Lung Adenocarcinoma Development.American journal of respiratory and critical care medicine · 2021Article
- Anti-Tumor Effects of Biomimetic Sulfated Glycosaminoglycans on Lung Adenocarcinoma Cells in 2D and 3D In Vitro Models.Molecules (Basel, Switzerland) · 2020Article
- Article
- ADAM17: An Emerging Therapeutic Target for Lung Cancer.Cancers · 2019Review
- Genome-Wide and Phenotypic Evaluation of Stem Cell Progenitors Derived FromFrontiers in oncology · 2019Article
- Clinical significance of reduced GPRC5A expression in surgically resected non-small cell lung cancer.Oncology letters · 2019Article
- Genome-Wide Gene Expression Changes in the Normal-Appearing Airway during the Evolution of Smoking-Associated Lung Adenocarcinoma.Cancer prevention research (Philadelphia, Pa.) · 2018Article
- Transcriptomic Alterations in Lung Adenocarcinoma Unveil New Mechanisms Targeted by theFrontiers in oncology · 2018Article
- GPRC5A: An Emerging Biomarker in Human Cancer.BioMed research international · 2018Review
- Development of Kras mutant lung adenocarcinoma in mice with knockout of the airway lineage-specific gene Gprc5a.International journal of cancer · 2017Article
- GPRC5A overexpression predicted advanced biological behaviors and poor prognosis in patients with gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- The emerging roles of GPRC5A in diseases.Oncoscience · 2014Review
- G-protein coupled receptor family C, group 5, member A (GPRC5A) expression is decreased in the adjacent field and normal bronchial epithelia of patients with chronic obstructive pulmonary disease and non-small-cell lung cancer.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundImproved understanding of lung cancer development and progression, including insights from studies of animal models, are needed to combat this fatal disease. Previously, we found that mice with a knockout (KO) of G-protein coupled receptor 5A (Gprc5a) develop lung tumors after a long latent period (12 to 24 months). METHODOLOGY/PRINCIPAL
findingsTo determine whether a tobacco carcinogen will enhance tumorigenesis in this model, we administered 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) i.p. to 2-months old Gprc5a-KO mice and sacrificed groups (n=5) of mice at 6, 9, 12, and 18 months later. Compared to control Gprc5a-KO mice, NNK-treated mice developed lung tumors at least 6 months earlier, exhibited 2- to 4-fold increased tumor incidence and multiplicity, and showed a dramatic increase in lesion size. A gene expression signature, NNK-ADC, of differentially expressed genes derived by transcriptome analysis of epithelial cell lines from normal lungs of Gprc5a-KO mice and from NNK-induced adenocarcinoma was highly similar to differential expression patterns observed between normal and tumorigenic human lung cells. The NNK-ADC expression signature also separated both mouse and human adenocarcinomas from adjacent normal lung tissues based on publicly available microarray datasets. A key feature of the signature, up-regulation of Ube2c, Mcm2, and Fen1, was validated in mouse normal lung and adenocarcinoma tissues and cells by immunohistochemistry and western blotting, respectively. CONCLUSIONS/SIGNIFICANCE: Our findings demonstrate that lung tumorigenesis in the Gprc5a-KO mouse model is augmented by NNK and that gene expression changes induced by tobacco carcinogen(s) may be conserved between mouse and human lung epithelial cells. Further experimentation to prove the reliability of the Gprc5a knockout mouse model for the study of tobacco-induced lung carcinogenesis is warranted.
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