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
Figure 5. Visfatin induced increases in VEGF-C expression and lymphangiogenesis by activating MEK1/2 signaling. (A, B) ESCC cells were treated with visfatin (30 ng/mL) for the indicated times and then MEK1/2 phosphorylation was examined by Western blot and quantified by ImageJ software. (C, D) ESCC cells were transfected or preincubated with the MEK1/2 inhibitor PD98059 or siRNAs for 24 h, before determining levels of VEGF-C expression by qPCR. (E) ESCC cells were transfected with MEK 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 MEK siRNA and MEK expression was examined by Western blot. *P < 0.05 compared with the control group; #P < 0.05 compared with the visfatin-treated group.