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. 2018 Jun 13;8(14):3824–3840. doi: 10.7150/thno.25308

Figure 4.

Figure 4

FTY720 in co-operation with gemcitabine inhibited cell proliferation and downregulated the activation of NF-kB and S1PR1/STAT3 pathways and PP2A activation in pancreatic cancer. (A) Immunohistochemical analysis of proliferative markers cyclin D1, β-catenin and Ki-67 in tissue samples (upper panel). The quantification positive cells are shown lower panel. (B) FTY treatment inhibited the activation of NF-κB and NF-κB dependent gene expression. Immunohistochemical analysis of nuclear translocation of p65, representative image (left panel) and quantification of nuclear positive cells (right panel). Statistical analysis was performed using one way ANOVA followed by post hoc Tukey test; * p≤0.001 vs control. (C) The circulatory TNF in serum was measured using ELISA. Statistical significance was calculated using t-test, * p≤0.001 vs control. (D) PP2A enzyme activity was measured using a commercially available kit. Statistical significance was calculated using t-test, ** p≤0.05 vs control. (E) FTY720 inhibited the S1PR1/STAT3 loop and downstream signaling in pancreatic cancer. Immunoblot analysis showing the expression of indicated proteins in tissue lysates of pancreatic cancer samples.