Fig. 4: EGF promoted the EMT process by activating the ERK1/2 pathway in HIBEpic cells.
From: Potential therapeutic target of EGF on bile duct ligation model and biliary atresia children
a Protein levels of p-ERK1/2 and p-NF-κB p65 increased 45 min after treatment with EGF. t-: total; p-: phosphorylated. b Protein levels of p-ERK1/2 increased by EGF treatment alone, and decreased after adding KO-947. c Protein levels of N-cadherin increased after EGF treatment, and decreased with the addition of KO-947. Opposite changes of E-cadherin were observed. d, e mRNA expression of E-cadherin (CDH1) decreased after EGF treatment and increased after KO-947 was added. Changes in N-cadherin (CDH2) were the opposite. *P < 0.05; ****P < 0.0001. f IF staining depicted that KO-947 inhibited the decreased fluorescence intensity of CK19 and increased fluorescence intensity of N-cadherin induced by EGF. (Scale bar: 100 μm) g IHC staining displayed that the expression of p-ERK1/2 and p-NF-κB p65 were significantly higher in biliary epithelial cells (black arrow), and slightly increased in hepatocytes of BA liver, compared with CC. (Magnification: left panel: ×200; right panel: ×400).
