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. 2021 Jun 15;22(6):492–503. doi: 10.1631/jzus.B2000842

Fig. 2. Janus kinase 2 (JAK2) inhibitor fedratinib causes a loss in the ability to suppress the survivals of MGC803, MIA PaCa-2, and PANC-1 cells via the inducement of extracellular signal-regulated kinase (ERK) signaling. (a) Fedratinib was added to MGC803, MIA PaCa-2, and PANC-1 cells at the indicated concentrations for 24 h. Cell viability was measured using a Cell Counting Kit-8 (CCK-8) assay. (b) MGC803 cells were treated with 5 μmol/L fedratinib at the indicated time points, and the tyrosine phosphorylation levels of EGFR, JAK2, and STAT3 were measured by western blot. (c) Fedratinib was added to MGC803 cells at different concentrations for 4 h, and the tyrosine phosphorylation levels of signal transducer and activator of transcription 3 (STAT3) and ERK were examined by western blot. (d) MIA PaCa-2 and PANC-1 cells were treated with fedratinib at different concentrations for 8 h, and the tyrosine phosphorylation levels of STAT3 and ERK were examined by western blot. The results are presented as the mean±standard deviation (SD) from three independent experiments. * P<0.05 and ** P<0.01 vs. control (no fedratinib).

Fig. 2