ArticleCancer prevention research (Philadelphia, Pa.)2010
Knockout of the tumor suppressor gene Gprc5a in mice leads to NF-kappaB activation in airway epithelium and promotes lung inflammation and tumorigenesis.
Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 84 citations in OpenAlex.
- G protein-coupled receptors as novel therapeutic targets in non-small-cell lung cancer.Medical review (2021) · 2025Review
- NF-κB-mediated EAAT3 upregulation in antioxidant defense and ferroptosis sensitivity in lung cancer.Cell death & disease · 2025Article
- Article
- Nuclear factor kappa B expression in non-small cell lung cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Review
- Integrating genomics and proteomics data to identify candidate plasma biomarkers for lung cancer risk among European descendants.British journal of cancer · 2023Article
- Upregulated GPRC5A disrupting the Hippo pathway promotes the proliferation and migration of pancreatic cancer cells via the cAMP-CREB axis.Discover oncology · 2023Article
- NF-κB represses retinoic acid receptor-mediated GPRC5A transactivation in lung epithelial cells to promote neoplasia.JCI insight · 2023Article
- IMUP and GPRC5A: two newly identified risk score indicators in pancreatic ductal adenocarcinoma.Cancer cell international · 2021Article
- Long noncoding RNA MIAT inhibits the progression of diabetic nephropathy and the activation of NF-κB pathway in high glucose-treated renal tubular epithelial cells by the miR-182-5p/GPRC5A axis.Open medicine (Warsaw, Poland) · 2021Article
- Mechanistic understanding of β-cryptoxanthin and lycopene in cancer prevention in animal models.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Review
- microRNA-367-3p regulation of GPRC5A is suppressed in ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- RAI3 is overexpressed in gastric adenocarcinoma but unrelated to prognosis.International journal of clinical and experimental pathology · 2019Article
- Identifying the localization and exploring a functional role for Gprc5c in the kidney.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Article
- GPRC5A: An Emerging Biomarker in Human Cancer.BioMed research international · 2018Review
- Orphan G protein-coupled receptor GPRC5A modulates integrin β1-mediated epithelial cell adhesion.Cell adhesion & migration · 2017Article
- Article
- Molecular Pathways: The Balance between Cancer and the Immune System Challenges the Therapeutic Specificity of Targeting Nuclear Factor-κB Signaling for Cancer Treatment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Review
- GPRC5A is a potential oncogene in pancreatic ductal adenocarcinoma cells that is upregulated by gemcitabine with help from HuR.Cell death & disease · 2016Article
- Caspase-9b Interacts Directly with cIAP1 to Drive Agonist-Independent Activation of NF-κB and Lung Tumorigenesis.Cancer research · 2016Article
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11 authors at 1 institution in 1 country.
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Abstract
Mouse models can be useful for increasing the understanding of lung tumorigenesis and assessing the potential of chemopreventive agents. We explored the role of inflammation in lung tumor development in mice with knockout of the tumor suppressor Gprc5a. Examination of normal lung tissue and tumors from 51 Gprc5a(+/+) (adenoma incidence, 9.8%; adenocarcinoma, 0%) and 38 Gprc5a(-/-) mice (adenoma, 63%; adenocarcinoma, 21%) revealed macrophage infiltration into lungs of 45% of the Gprc5a(-/-) mice and 8% of Gprc5a(+/+) mice and the direct association of macrophages with 42% of adenomas and 88% of adenocarcinomas in the knockout mice. Gprc5a(-/-) mouse lungs contained higher constitutive levels of proinflammatory cytokines and chemokines and were more sensitive than lungs of Gprc5a(+/+) mice to stimulation of NF-kappaB activation by lipopolysaccharide in vivo. Studies with epithelial cells cultured from tracheas of Gprc5a(-/-) and Gprc5a(+/+) mice revealed that Gprc5a loss is associated with increased cell proliferation, resistance to cell death in suspension, and increased basal, tumor necrosis factor alpha-induced, and lipopolysaccharide-induced NF-kappaB activation, which were reversed partially in Gprc5a(-/-) adenocarcinoma cells by reexpression of Gprc5a. Compared with Gprc5a(+/+) cells, the Gprc5a(-/-) cells produced higher levels of chemokines and cytokines and their conditioned medium induced more extensive macrophage migration. Silencing Gprc5a and the p65 subunit of NF-kappaB in Gprc5a(+/+) and Gprc5a(-/-) cells, respectively, reversed these effects. Thus, Gprc5a loss enhances NF-kappaB activation in lung epithelial cells, leading to increased autocrine and paracrine interactions, cell autonomy, and enhanced inflammation, which may synergize in the creation of a tumor-promoting microenvironment.
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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.