Research Paper Volume 13, Issue 14 pp 18545—18563

The anti-dysenteric drug fraxetin enhances anti-tumor efficacy of gemcitabine and suppresses pancreatic cancer development by antagonizing STAT3 activation

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Figure 6. Reactivation of STAT3 reverses the anti-tumor effects of fraxetin. (A) The proliferation of fraxetin-treated PANC-1 and Patu8988 cells with or without colivelin treatment was analyzed by colony formation assay. (B) The transwell chamber assay analyzed the invasion ability of fraxetin-treated PANC-1 and Patu8988 cells with or without colivelin treatment. (C) A wound healing assay was used to determine the migration ability of fraxetin-treated PANC-1 and Patu8988 cells with or without colivelin treatment. (D) E-cadherin and Slug expression in fraxetin-treated PANC-1 and Patu8988 cells with and without colivelin treatment, as determined by Western blot analysis. (E) Immunocytochemical staining of E-cadherin in fraxetin-treated PANC-1 and Patu8988 cells with or without colivelin treatment. Bar = 25 μm. (F) N-cadherin and Type I collagen expression in fraxetin-treated PANC-1 and Patu8988 cells with and without colivelin treatment, as determined by Western blot analysis. (G) Immunocytochemical staining of vimentin in fraxetin-treated PANC-1 and Patu8988 cells with or without colivelin treatment. Bar = 25 μm. Data were presented as the mean ± standard deviation, and were analyzed by One-way ANOVA with Bonferroni’s post-hoc test and two-sided Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001.