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Fig. 6 | Parasites & Vectors

Fig. 6

From: Clonorchis sinensis granulin promotes malignant transformation of human intrahepatic biliary epithelial cells through interaction with M2 macrophages via regulation of STAT3  phosphorylation and the MEK/ERK pathway

Fig. 6

ae Mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) was involved in the malignant proliferation and metastasis of HIBECs caused by CsGRN-mediated cell–cell interaction. a The expression of phosphorylated (p-) MEK (p-MEK) and p-ERK in the co-culture medium (Fig. 5) and with MEK/ERK inhibitor co-culture medium (b) were assessed by western blot. c The expression of p-MEK+ CK19+ cells and p-ERK+ CK19+ cells in the liver of CsGRN-injected mice were assessed by IF. Scale bar 100 μM. EdU-488 assay (d) and Transwell assay (e) were performed to evaluate the migration or proliferation of HIBECs after treatment with MEK/ERK inhibitor. Scale bar 10 μM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. For other abbreviations, see Figs. 1, 2 and  3 and 4

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