ArticleThe Journal of biological chemistry2011
Enhanced epithelial-mesenchymal transition-like phenotype in N-acetylglucosaminyltransferase V transgenic mouse skin promotes wound healing.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 65 citations in OpenAlex.
- Role of the GalNAc-galectin pathway in the healing of premature rupture of membranes.Molecular medicine (Cambridge, Mass.) · 2024Article
- Aberrant N-glycosylation in cancer: MGAT5 and β1,6-GlcNAc branched N-glycans as critical regulators of tumor development and progression.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- Role of glycosyltransferases in carcinogenesis; growth factor signaling and EMT/MET programs.Glycoconjugate journal · 2022Review
- Identification of glycogene signature as a tool to predict the clinical outcome and immunotherapy response in breast cancer.Frontiers in oncology · 2022Article
- Glycobiology of the Epithelial to Mesenchymal Transition.Biomedicines · 2021Review
- Fibroblast growth factor 2 accelerates the epithelial-mesenchymal transition in keratinocytes during wound healing process.Scientific reports · 2020Article
- Partial silencing of fucosyltransferase 8 gene expression inhibits proliferation of Ishikawa cells, a cell line of endometrial cancer.Biochemistry and biophysics reports · 2020Article
- Regulatory T Cells Conditioned Media Stimulates Migration in HaCaT Keratinocytes: Involvement of Wound Healing.Clinical, cosmetic and investigational dermatology · 2020Article
- Helium/Argon-Generated Cold Atmospheric Plasma Facilitates Cutaneous Wound Healing.Frontiers in bioengineering and biotechnology · 2020Article
- Non-redundant functions of EMT transcription factors.Nature cell biology · 2019Review
- The role of the epithelial-to-mesenchymal transition (EMT) in diseases of the salivary glands.Histochemistry and cell biology · 2018Review
- N-glycosylation by N-acetylglucosaminyltransferase V enhances the interaction of CD147/basigin with integrin β1 and promotes HCC metastasis.The Journal of pathology · 2018Article
- Re-evaluating the role of epithelial-mesenchymal-transition in cancer progression.Journal of biomedical research · 2018Article
- Epithelial-to-mesenchymal transition in cutaneous wound healing: Where we are and where we are heading.Developmental dynamics : an official publication of the American Association of Anatomists · 2018Review
- Epithelial-mesenchymal transition in tissue repair and fibrosis.Cell and tissue research · 2016Review
- N-Acetylglucosaminyltransferase V exacerbates murine colitis with macrophage dysfunction and enhances colitic tumorigenesis.Journal of gastroenterology · 2016Article
- Loss of Mgat5a-mediatedCell regeneration (London, England) · 2016Article
- Epithelial-mesenchymal transition: An emerging target in tissue fibrosis.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- Remodeling of epithelial cells and basement membranes in a corneal deficiency model with long-term follow-up.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Molecular basis for MMP9 induction and disruption of epithelial cell-cell contacts by galectin-3.Journal of cell science · 2014Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-Acetylglucosaminyltransferase V (GnT-V) catalyzes the β1,6 branching of N-acetylglucosamine on N-glycans. GnT-V expression is elevated during malignant transformation in various types of cancer. However, the mechanism by which GnT-V promotes cancer progression is unclear. To characterize the biological significance of GnT-V, we established GnT-V transgenic (Tg) mice, in which GnT-V is regulated by a β-actin promoter. No spontaneous cancer was detected in any organs of the GnT-V Tg mice. However, GnT-V expression was up-regulated in GnT-V Tg mouse skin, and cultured keratinocytes derived from these mice showed enhanced migration, which was associated with changes in E-cadherin localization and epithelial-mesenchymal transition (EMT). Further, EMT-associated factors snail, twist, and N-cadherin were up-regulated, and cutaneous wound healing was accelerated in vivo. We further investigated the detailed mechanisms of EMT by assessing EGF signaling and found up-regulated EGF receptor signaling in GnT-V Tg mouse keratinocytes. These findings indicate that GnT-V overexpression promotes EMT and keratinocyte migration in part through enhanced EGF receptor signaling.
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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.