ArticleInvestigative ophthalmology & visual science2012
Role of CTCF in EGF-induced migration of immortalized human corneal epithelial cells.
Article in Investigative ophthalmology & visual science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- High-resolution promoter map of human limbal epithelial cells cultured with keratinocyte growth factor and rho kinase inhibitor.Scientific reports · 2017Article
- CTCF-Mediated and Pax6-Associated Gene Expression in Corneal Epithelial Cell-Specific Differentiation.PloS one · 2016Article
- Progress in corneal wound healing.Progress in retinal and eye research · 2015Review
- Epidermal growth factor (EGF)-induced corneal epithelial wound healing through nuclear factor κB subtype-regulated CCCTC binding factor (CTCF) activation.The Journal of biological chemistry · 2013Article
- Ocular surface development and gene expression.Journal of ophthalmology · 2013Article
- Corneal epithelial development and homeostasis.Differentiation; research in biological diversityReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeEGF-induced activation of the epigenetic CCCTC binding factor (CTCF) plays an important role in corneal epithelial cell proliferation by suppressing the Pax6 gene. The present study focused on further understanding the role of CTCF in mediating EGF-induced migration of immortalized human corneal epithelial cells.
methodsCTCF activities in human corneal epithelial cells immortalized by telomerase (HTCE cells) and SV-40 (HCE cells) transformation were suppressed and enhanced by CTCF mRNA knockdown and by overexpressing CTCF cDNA, respectively. EGF-induced cell migration was evaluated by linear scratch wound healing, a cell migration assay, and live cell motility GFP-tracking with a fluorescence microscope. Immunochemical analysis was performed for detecting focal adhesion changes in EGF-induced and CTCF activity-altered cells.
resultsEGF-induced wound closure and cell migration rates of human corneal epithelial cells were significantly suppressed and enhanced by CTCF mRNA knockdown and by overexpression of CTCF, respectively. CTCF mRNA knockdown also markedly suppressed cell motility, determined by using a live-cell-tracking system in GFP-tag-expressed HTCE cells. Finally, alterations of EGF-stimulated focal adhesion were observed in CTCF knockdown HTCE cells by immunostaining of F-actin and vinculin in cytoskeleton reorganization.
conclusionsCTCF, an epigenetic regulator and transcription factor, involves EGF-induced increases in cell motility and migration. CTCF plays an essential role in growth factor-regulated human corneal epithelial cell wound healing.
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Registered trials
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