Fig. 3: Vortioxetine hydrobromide suppressed STAT3 signaling pathway by targeting JAK2 and SRC kinases.

A In vitro kinase assay of active JAK2 and inactive STAT3. The active JAK2, inactive STAT3, and ATP mixture were treated with vortioxetine hydrobromide or DMSO at 30 °C for 30 min. p-STAT3 Y705 and STAT3 were visualized by Western blotting. B Vortioxetine hydrobromide suppressed SRC kinase activity in a dose-dependent manner. C The protein levels of JAK2/SRC-STAT3 signaling pathway in GC cells after vortioxetine hydrobromide (0, 0.5, 1, 2, 4 μM) treatment. The quantitative analyses of fluorescence intensity of p-STAT3 (D) and STAT3 (E) in GC cells. F The changes of STAT3 dimer formation after vortioxetine hydrobromide treatment in GC cells. G The nucleus localization variation of STAT3 after treatment of various concentrations of vortioxetine hydrobromide in HGC27 cells. H The protein levels of Bcl2, Mcl1 and c-Myc by Western blotting after treatment of various concentrations of vortioxetine hydrobromide in HGC27 cells. Mean ± S.D. (n = 3) (*p < 0.05, **p < 0.01, ***p < 0.001).