Research Paper Volume 15, Issue 11 pp 4774—4793

Visfatin upregulates VEGF-C expression and lymphangiogenesis in esophageal cancer by activating MEK1/2-ERK and NF-κB signaling

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Figure 7. Visfatin induced increases in VEGF-C expression and lymphangiogenesis by activating NF-κB signaling. (A, B) ESCC cells were treated with visfatin (30 ng/mL) for the indicated times and then p65 phosphorylation was examined by Western blot and quantified by ImageJ software. (C, D) ESCC cells were transfected or preincubated with NF-κB inhibitors (PDTC and TPCK) or siRNAs for 24 h and then VEGF-C expression levels were measured by qPCR. (E) ESCC cells were transfected with p65 siRNA for 24 h, then stimulated with visfatin (30 ng/mL) for 24 h. Levels of VEGF-C expression were examined by Western blot. (F) ESCCs were transfected with a p65 siRNA and p65 expression was examined by Western blot. (G) ESCCs were treated with MEK and ERK inhibitors then stimulated with visfatin, and NF-κB luciferase activity was examined. *P < 0.05 compared with the control group; #P < 0.05 compared with the visfatin-treated group.