Fig. 4: PA28γ-dependent upregulation of phosphorylated MEK1 promotes EMT in epithelial cells. | Cell Death & Disease

Fig. 4: PA28γ-dependent upregulation of phosphorylated MEK1 promotes EMT in epithelial cells.

From: Identification of a BRAF/PA28γ/MEK1 signaling axis and its role in epithelial-mesenchymal transition in oral submucous fibrosis

Fig. 4: PA28γ-dependent upregulation of phosphorylated MEK1 promotes EMT in epithelial cells.

A, B Wound healing and transwell assays showed that epithelial cells overexpressing PA28γ by lentivirus acquired enhanced migration capacity, which could be reduced by knocking down PA28γ or MEK1 expression. Scale bar: 100 μm. C, D Data represent the means ± s.d. of three independent experiments. Statistical analysis was performed using Student’s t test (***p < 0.001, ****p < 0.000). E Immunostaining and F western blot assays showed that overexpressed PA28γ led cells to acquire a mesenchymal phenotype with higher Vimentin expression and lower E-cadherin expression. Knocking down MEK1 in epithelial cells stably overexpressing PA28γ partly reversed the EMT phenotype. Scale bar: 50 μm.

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