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. 2021 Feb 26;42(7):940–950. doi: 10.1093/carcin/bgab017

Figure 3.

Figure 3.

DPYD and pSTAT3 expression affected one other. Western blotting for pSTAT3, STAT3, DPYD and β-Actin protein in nine human pancreatic cell lines (A). DPYD and pSTAT3 expression corrected by β-Actin and total STAT3 (Spearman rho = 0.883, P < 0.01) (B). Western blotting for pSTAT3, STAT3, DPYD and β-Actin after Lut (25, 50 μM) or Stattic (5 μM) treatment in the DPYD high-expressing line (KP4) (C) and after stimulation of the STAT3 pathway by IL 6 (50 ng/ml) for 24 h followed by addition of Lut (10, 25, 50 μM) in a DPYD low-expressing line (AsPC1) (D). Expression of DPYD mRNA (n = 3 per cell) (E) and DPYD protein for pSTAT3, STAT3, Cyclin D1 and β-Actin (F), and cell proliferation (n = 6 per condition) (G) after siDPYD (siDPYD1, siDPYD2) transfection into KP4 cells. Expression of DPYD, pSTAT3, STAT3 and β-Actin protein (H, I) and proliferation (J, K) when DPYD is overexpressed with or without Stattic treatment in AsPC1 and PATU-8988T cells (MIAPaCa cell protein as a positive control for DPYD). Data are mean ± SD. *, **, *** P < 0.001 compared with control or siControl or CSII-LacZ.