ArticleNeoplasia (New York, N.Y.)2012
E-cadherin controls bronchiolar progenitor cells and onset of preneoplastic lesions in mice.
Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- The clinicopathological significance and potential drug target of E-cadherin in NSCLC.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Pooled it
- Disruption of E-cadherin in the airway led to dysplastic stressed cells and asthma-like phenotypes.Developmental cell · 2025Article
- Contribution of the bitter taste signaling pathway to lung inflammation duringFrontiers in immunology · 2025Article
- Conditional knockout of ITGB4 in bronchial epithelial cells directs bronchopulmonary dysplasia.Journal of cellular and molecular medicine · 2023Article
- Fungal Aeroallergens-The Impact of Climate Change.Journal of fungi (Basel, Switzerland) · 2023Review
- Network analyses of upper and lower airway transcriptomes identify shared mechanisms among children with recurrent wheezing and school-age asthma.Frontiers in immunology · 2023Article
- Integrin-β4 regulates the dynamic changes of phenotypic characteristics in association with epithelial-mesenchymal transition (EMT) and RhoA activity in airway epithelial cells during injury and repair.International journal of biological sciences · 2022Article
- Deficiency of IntegrinFrontiers in cell and developmental biology · 2022Article
- Inhibition of β-Catenin/CREB Binding Protein Signaling Attenuates House Dust Mite-Induced Goblet Cell Metaplasia in Mice.Frontiers in physiology · 2021Article
- Review
- Epithelial barriers in allergy and asthma.The Journal of allergy and clinical immunology · 2020Review
- Characterization of a lung epithelium specific E-cadherin knock-out model: Implications for obstructive lung pathology.Scientific reports · 2018Article
- ITGB4 deficiency in bronchial epithelial cells directs airway inflammation and bipolar disorder-related behavior.Journal of neuroinflammation · 2018Article
- Signal transduction growth factors: the effective governance of transcription and cellular adhesion in cancer invasion.Oncotarget · 2017Review
- The role and importance of club cells (Clara cells) in the pathogenesis of some respiratory diseases.Kardiochirurgia i torakochirurgia polska = Polish journal of cardio-thoracic surgery · 2016Article
- Intracellular signals of lung cancer cells as possible therapeutic targets.Cancer science · 2015Review
- Cancer subclonal genetic architecture as a key to personalized medicine.Neoplasia (New York, N.Y.) · 2013Article
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
- Short histological kaleidoscope - recent findings in histology. Part IV.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although progenitor cells of the conducting airway have been spatially localized and some insights have been gained regarding their molecular phenotype, relatively little is known about the mechanisms regulating their maintenance, activation, and differentiation. This study investigates the potential roles of E-cadherin in mouse Clara cells, as these cells were shown to represent the progenitor/stem cells of the conducting airways and have been implicated as the cell of origin of human non-small cell lung cancer. Postnatal inactivation of E-cadherin affected Clara cell differentiation and compromised airway regeneration under injury conditions. In steady-state adult lung, overexpression of the dominant negative E-cadherin led to an expansion of the bronchiolar stem cells and decreased differentiation concomitant with canonical Wnt signaling activation. Expansion of the bronchiolar stem cell pool was associated with an incessant proliferation of neuroepithelial body.associated Clara cells that ultimately gave rise to bronchiolar hyperplasia. Despite progressive hyperplasia, only a minority of the mice developed pulmonary solid tumors, suggesting that the loss of E-cadherin function leads to tumor formation when additional mutations are sustained. The present study reveals that E-cadherin plays a critical role in the regulation of proliferation and homeostasis of the epithelial cells lining the conducting airways.
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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.