| First Author | Terao M | Year | 2011 |
| Journal | J Biol Chem | Volume | 286 |
| Issue | 32 | Pages | 28303-11 |
| PubMed ID | 21697088 | Mgi Jnum | J:175920 |
| Mgi Id | MGI:5287933 | Doi | 10.1074/jbc.M111.220376 |
| Citation | Terao M, et al. (2011) Enhanced epithelial-mesenchymal transition-like phenotype in N-acetylglucosaminyltransferase V transgenic mouse skin promotes wound healing. J Biol Chem 286(32):28303-11 |
| abstractText | N-Acetylglucosaminyltransferase V (GnT-V) catalyzes the beta1,6 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 beta-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. |
