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 4. Fraxetin enhanced the sensitivity of PCCs to gemcitabine. (A, B) By using a colony formation assay, the effects of fraxetin on the proliferation of gemcitabine-treated PANC-1 cells were investigated. (C, D) A wound healing assay was used to determine the effects of fraxetin on the migrated rate of gemcitabine-treated PANC-1 cells. (E, F) The transwell chamber assay was used to examine the effects of fraxetin on the invasion number of gemcitabine-treated PANC-1 cells. (G) Immunocytochemical staining of N-cadherin and Vimentin in gemcitabine-treated PANC-1 with or without fraxetin treatment. Bar = 50 μm. (H) N-cadherin and Vimentin expression in gemcitabine-treated PANC-1 with or without fraxetin treatment, as determined by Western blot analysis. 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 < 0.001.