ArticleJournal of cell science2010
Aberrant expression of a beta-catenin gain-of-function mutant induces hyperplastic transformation in the mouse cornea.
Article in Journal of cell science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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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.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Bone morphogenetic protein 4 thermosensitive hydrogel inhibits corneal neovascularization by repairing corneal epithelial apical junctional complexes.Materials today. Bio · 2024Article
- Generation and characterization of Aldh3-Cre transgenic mice as a tool for conditional gene deletion in postnatal cornea.Scientific reports · 2020Article
- Shp2-mediated MAPK pathway regulates ΔNp63 in epithelium to promote corneal innervation and homeostasis.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Aberrant expression of a stabilized β-catenin mutant in keratocytes inhibits mouse corneal epithelial stratification.Scientific reports · 2019Article
- Transformation of the Transcriptomic Profile of Mouse Periocular Mesenchyme During Formation of the Embryonic Cornea.Investigative ophthalmology & visual science · 2019Article
- Antifibrotic Actions of Peroxisome Proliferator-Activated Receptor γ Ligands in Corneal Fibroblasts Are Mediated by β-Catenin-Regulated Pathways.The American journal of pathology · 2017Article
- KLF4 Plays an Essential Role in Corneal Epithelial Homeostasis by Promoting Epithelial Cell Fate and Suppressing Epithelial-Mesenchymal Transition.Investigative ophthalmology & visual science · 2017Article
- Foxc1 and Foxc2 in the Neural Crest Are Required for Ocular Anterior Segment Development.Investigative ophthalmology & visual science · 2017Article
- SFRP1 is a possible candidate for epigenetic therapy in non-small cell lung cancer.BMC medical genomics · 2016Article
- Expression of retinoic acid-binding proteins and retinoic acid receptors in sebaceous cell carcinoma of the eyelids.BMC ophthalmology · 2015Article
- Wnt/β-catenin signaling modulates corneal epithelium stratification via inhibition of Bmp4 during mouse development.Development (Cambridge, England) · 2015Article
- Disruption of eyelid and cornea morphogenesis by epithelial β-catenin gain-of-function.Molecular vision · 2015Article
- Overexpression of Pax6 in mouse cornea directly alters corneal epithelial cells: changes in immune function, vascularization, and differentiation.Investigative ophthalmology & visual science · 2011Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
Beta-catenin signaling has been shown to play a fundamental role in embryonic development and tumorigenesis. In this study, we investigated the role of beta-catenin (Ctnnb1) in corneal homeostasis and tumorigenesis. Conditional expression of a murine Ctnnb1 gain-of-function mutation alone caused corneal neoplasia and neovascularization, resembling human ocular surface squamous neoplasia (OSSN). These corneas displayed an upregulation of cell proliferative markers (PCNA and p63), while presenting downregulation of both the Pax-6 transcription factor and the corneal differentiation marker cytokeratin 12. In addition, the expression of limbal-type keratin 15 ectopically extended to cornea, but the pattern of conjunctival keratin 4 and epidermal keratin 10 were unchanged. Moreover, epithelial E-cadherin and laminins decreased concomitantly with elevated levels of MMP-7. We also noticed a dramatic upregulation of pro-angiogenic factors (Vegf-A, Vegfr1) and angiopoietins in these corneas. Interestingly, all human OSSN specimens examined revealed nuclear beta-catenin immunoreactivity. Taken together, these results argue that beta-catenin activation is a crucial step during OSSN pathogenesis. Thus, inhibition of beta-catenin might be beneficial for treating this disease.
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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.