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. 2016 Feb 12;7(10):11708–11723. doi: 10.18632/oncotarget.7336

Figure 3. Lip-FLLL32 inhibits pancreatic cancer cell growth in vitro in a STAT3 dependent way.

Figure 3

(A) Western blot analysis of total STAT3, pSTAT3 and its target proteins in PANC-1 cells treated with 5 μM FLLL32 or Lip-FLLL32 at indicated time points. β-Actin was used as loading control. (B) STAT3-dependent transcriptional luciferase activity assay in PANC-1 cells treated with FLLL32 or Lip-FLLL32. PANC-1 cells were co-transfected with pLucTKS3 luciferase reporter construct and beta-galactosidase plasmid, and then treated with FLLL32 or Lip-FLLL32 for 24 hours. Values are mean ± SD from two independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, one-way ANOVA. (C) The cytotoxicity of free FLLL32 (left) and Lip-FLLL32 (right) against BxPC-3, PANC-1 and WI-38 cell lines. (D) Colony formation assay in PANC-1 (left) and BxPC-3 (right) cells treated with free FLLL32 or lip-FLLL32 at indicated doses. DMSO was used as vehicle control of FLLL32 and Lip only was used as vehicle control of Lip-FLLL32. *P < 0.05, **P < 0.01, ***P < 0.001, two-way ANOVA.