Enhancement of Epitelial-Mesenchymal Transition-Like Phenotype in N-acetylglucosaminyltransferase V Transgenic Mouse Skin Promotes Wound Healing

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 upregulated 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 upregulated, and cutaneous wound healing was accelerated in vivo. We further investigated the detailed mechanisms of EMT by assessing epidermal growth factor (EGF) signaling and found upregulated 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.