西亚试剂：Np63α Protein Triggers Epithelial-Mesenchymal Transition an

Np63α Protein Triggers Epithelial-Mesenchymal Transition and Confers Stem Cell Properties in Normal Human Keratinocytes

Ju-Eun Oh, Reuben H. Kim, Ki-Hyuk Shin, No-Hee Park, and Mo K. Kang

p63 is a p53 family protein required for morphogenesis and postnatal regeneration of epithelial tissues. Here we demonstrate that Np63α, a p63 isoform lacking the N-terminal transactivation domain, induces epithelial-mesenchymal transition (EMT) in primary human keratinocytes in a TGF-β-dependent manner. Rapidly proliferating normal human epidermal keratinocytes (NHEK) were infected with retroviral vector expressing Np63α or empty vector and serially subcultured until replicative senescence. No phenotypic changes were observed until the culture reached senescence. Then the Np63α-transduced cells underwent morphological changes resembling mesenchymal cells and acquired the EMT phenotype. Treatment with exogenous TGF-β accelerated EMT in presenescent Np63α-transduced cells, whereas the inhibition of TGF-β signaling reversed the EMT phenotype. TGF-β treatment alone led to growth arrest in control NHEK with no evidence of EMT, indicating that Np63α altered the cellular response to TGF-β treatment. Np63α-transduced cells acquiring EMT gained the ability to be differentiated to osteo-/odontogenic and adipogenic pathways, resembling mesenchymal stem cells. Furthermore, these cells expressed enhanced levels of Nanog and Lin28, which are transcription factors associated with pluripotency. These data indicate that EMT required Np63α transduction and intact TGF-β signaling in NHEK.

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