ArticleMolecular cancer2012
Enhancement of lung tumorigenesis in a Gprc5a Knockout mouse by chronic extrinsic airway inflammation.
Article in Molecular cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Association between the oral microbiome and clinical indicators of resectable non-small cell lung cancer (NSCLC).Journal of oral microbiology · 2026Article
- The role and mechanisms of the HIF-1 signaling pathway in LC-COPD.Journal of cancer research and clinical oncology · 2025Review
- Deciphering the molecular regulatory of RAB32/GPRC5A axis in chronic obstructive pulmonary disease.Respiratory research · 2024Article
- The Role ofWorld journal of oncology · 2023Article
- NF-κB represses retinoic acid receptor-mediated GPRC5A transactivation in lung epithelial cells to promote neoplasia.JCI insight · 2023Article
- Pulmonary Inflammation and KRAS Mutation in Lung Cancer.Advances in experimental medicine and biology · 2021Article
- Clinical significance of reduced GPRC5A expression in surgically resected non-small cell lung cancer.Oncology letters · 2019Article
- Bronchoalveolar Lavage Fluid-Derived Exosomes: A Novel Role Contributing to Lung Cancer Growth.Frontiers in oncology · 2019Article
- Effect of a 12-week submaximal swimming training in rats exposed to tobacco- derived nitrosamine ketone.Caspian journal of internal medicine · 2018Article
- Non-typeableMultidisciplinary respiratory medicine · 2018Article
- GPRC5A: An Emerging Biomarker in Human Cancer.BioMed research international · 2018Review
- 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
- Epithelial neoplasia coincides with exacerbated injury and fibrotic response in the lungs of Gprc5a-knockout mice following silica exposure.Oncotarget · 2015Article
- Large-scale RNA-Seq Transcriptome Analysis of 4043 Cancers and 548 Normal Tissue Controls across 12 TCGA Cancer Types.Scientific reports · 2015Article
- Differential Cytotoxicity but Augmented IFN-γ Secretion by NK Cells after Interaction with Monocytes from Humans, and Those from Wild Type and Myeloid-Specific COX-2 Knockout Mice.Frontiers in immunology · 2015Article
- The regulation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumor promotion by estradiol in female A/J mice.PloS one · 2014Article
- Silica-induced chronic inflammation promotes lung carcinogenesis in the context of an immunosuppressive microenvironment.Neoplasia (New York, N.Y.) · 2013Article
- Expression and significance of HMGB1, TLR4 and NF-κB p65 in human epidermal tumors.BMC cancer · 2013Article
- 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
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlthough cigarette smoking is the principal cause of lung carcinogenesis, chronic obstructive pulmonary disease (COPD), an inflammatory disease of the lung, has been identified as an independent risk factor for lung cancer. Bacterial colonization, particularly with non-typeable Haemophilus influenzae (NTHi), has been implicated as a cause of airway inflammation in COPD besides cigarette smoke. Accordingly, we hypothesized that lung cancer promotion may occur in a chronic inflammatory environment in the absence of concurrent carcinogen exposure.
resultsHerein, we investigated the effects of bacterial-induced COPD-like inflammation and tobacco carcinogen-enhanced tumorigenesis/inflammation in the retinoic acid inducible G protein coupled receptor knock out mouse model (Gprc5a-/- mouse) characterized by late-onset, low multiplicity tumor formation. Three-month-old Gprc5a-/- mice received 4 intraperitoneal injections of the tobacco-specific carcinogen, NNK, followed by weekly exposure to aerosolized NTHi lysate for 6 months. The numbers of inflammatory cells in the lungs and levels of several inflammatory mediators were increased in Gprc5a-/- mice treated with NTHi alone, and even more so in mice pretreated with NNK followed by NTHi. The incidence of spontaneous lung lesions in the Gprc5a-/- mice was low, but NTHi exposure led to enhanced development of hyperplastic lesions. Gprc5a-/- mice exposed to NNK alone developed multiple lung tumors, while NTHi exposure increased the number of hyperplastic foci 6-fold and the tumor multiplicity 2-fold. This was associated with increased microvessel density and HIF-1α expression.
conclusionWe conclude that chronic extrinsic lung inflammation induced by bacteria alone or in combination with NNK enhances lung tumorigenesis in Gprc5a-/- mice.
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